Cardiovascular 'reactivity' to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats.

Cardiovascular 'reactivity' to graded splanchnic nerve stimulation was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/ri of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.     

Interaction between “mental stress” and baroreceptor reflexes concerning effects on heart rate,mean arterial pressure and renal sympathetic activity in conscious spontaneously hypertensive rats

Spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared concerning the interactions between cortico-hypothalamic alerting responses and baroreflex influences on neurogenic cardiovascular control. For this purpose mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were continuously recorded during night time in conscious, otherwise undisturbed rats. Baroreceptor sensitivity was assessed as percentage HR and RSNA reductions per mmHg MAP elevation when a standardized phenylephrine infusion was performed. A state of acute “mental stress” could be induced by a likewise standardized sudden blowing of air. These two opposing influences on neurogenic cardiovascular control were also experimentally superimposed in various ways and the effects on MAP, HR and RSNA followed. During “rest” RSNA was higher in SHR than in WKY and it also increased more during “mental stress”. The baroreflex sensitivity was clearly reduced in SHR and WKY concerning HR reduction (0.44±0.06 vs. 0.78±0.08%/mmHg; p<0.01) but not so concerning RSNA, which was similar in SHR and WKY (2.6±0.2 vs. 2.9±0.4%/mmHg). If expressed (HR + 1±3%; p<0.025 vs. SHR and RSNA + 11%±10, p<0.01 vs. SHR). These results) (0.10±0.02 vs. 0.06±0.01 μV/mmHg; p<0.12). Also single fibre recordings in anaesthetized rats showed the same principle difference between SHR and WKY. Addition of “mental stress” during phenylephrine baroreflex activation clearly increased both HR (24±7%) and RSNA (114±21 %) in SHR, while almost no change then occurred in WKY (HR + 1±3%; p<0.025 vs. SHR and RSNA + 11%±10, p<0.01 vs. SHR). These results suggest that a modestly accentuated cortico-hypothalamic activity ordinarily prevails in SHR, explaining the suppressed baroreflex control of heart rate and the augmented sympathetic activity to e.g. renal and splanchnic areas. Further, environmental alerting stimuli induce in SHR more powerful defence reactions which, unlike the situation in WKY, readily overcome baroreflex inhibitory influences on sympathetic activity.     

Altered hemodynamic responses to acute hypoxemia in spontaneously hypertensive rats.

Conscious spontaneously hypertensive rats (SHR), 5--7 wk old, were studied hemodynamically by the direct Fick procedure to determine whether high total peripheral resistance (TPR) coexisted with increased oxygen consumption (QO2) at an early stage of hypertension development. Since under resting conditions cardiac output in SHR was not significantly different from normotensive controls, the elevated arterial pressure and QO2 were associated with increased TPR. Arterial hypoxemia was induced to reduce oxygen availability and to assess whether increased TPR in SHR could be reversed by this procedure. During hypoxemia, normotensive controls (WKY) responded with increased cardiac output and decreased arterial pressure and TPR. In contrast, arterial pressure and cardiac output fell in SHR; and the increased TPR persisted. QO2 fell in hypoxemic SHR demonstrating that the relationship between total body oxygen consumption and cardiac output was abnormal in young SHR, and that increased TPR in SHR was not dependent on resting levels of QO2 or oxygen availability. Although QO2 was elevated in SHR compared to age-matched WKY, this condition was not essential for maintained elevated vascular resistance.     

Cardiovascular and hormonal responses to static handgrip in young and older healthy men

The purpose of this study was to investigate the effect of age on cardiovascular changes and plasma concentrations of adrenomedullin (ADM), catecholamines, endothelin-1 (ET-1) and plasma renin activity (PRA) in healthy men. A total of 15 young (21 ± 0.3 years) and 15 older (64 ± 0.7 years) healthy men performed two 3-min bouts of static handgrip at 30% of maximal voluntary contraction, alternately with each hand without any break between the bouts. During exercise heart rate (HR), blood pressure (BP), stroke volume (SV) and pre-ejection period (PEP) and left ventricle ejection time (LVET) were measured. Blood samples were taken before exercise, at the end of both exercise bouts and in the fifth minute of the recovery period. The handgrip-induced increases in HR and cardiac output were significantly smaller in older than in young men (p < 0.01). SV decreased only in older men (p < 0.001). There were no differences between groups in BP increases. The baseline plasma ADM and catecholamines were higher in older man compared to young subjects. Handgrip caused increases in plasma ADM, ET-1 and PRA only in older men (p < 0.05). The increases in plasma ADM correlated positively with those of noradrenaline (NA), PRA, ET-1 and LVET and negatively with changes in total peripheral resistance (TPR), SV, PEP and PEP/LVET ratio. The increases in plasma ET-1 correlated positively with those of NA, PRA, TPR, mean BP and SV. These results revealed that ADM, ET-1 and angiotensin II can contribute to maintain vascular tone during static exercise in older but not in younger men.     

Influences on central hemodynamics in hemorrhage of β2-adrenergic vascular control mechanisms

Central hemodynamic responses evoked by standardized hemorrhage (exsanguination of 20 ml×kg bwt^-1) were followed during 2 h in cats with intact and blocked vascular β₂-adrenoceptors using the ‘selective’β₂-blocker, ICI 118, 551. In the first 10 min after bleeding blood pressure and cardiac output (CO) decreased and total peripheral resistance (TPR) increased by the same amount in the ‘intact’ and β₂-blocked animals. Whereas blood pressure later on reached approximately the same hypotension level in both groups, other hemodynamic variables were distinctly different. In the ‘intact’ animals there was a gradual, partial recovery of stroke volume (SV) and CO in the face of a restoration to control of TPR. In the β₂-blocked animals TPR continued to increase in the face of a maintained low CO and declining SV. The lower SV in the latter group was ascribed to abolition of β₂-adrenergic restoration of plasma volume via absorption of tissue fluid into the circulation. The gradual decline of TPR in the ‘intact’ animals was attributed to β₂-adrenergic dilator interaction with constrictor influences on the resistance vessels. It is concluded that β-adrenergic vascular control mechanisms help to improve nutritional tissue blood flow during hemorrhage by increasing plasma volume, and hence venous return and CO, and by decreasing TPR. These reflex, β₂-adrenergic circulatory events are similar to those aimed at in current shock therapy by transfusion and vasodilator treatment.     

The effects of varying sodium diets on haemodynamics and fluid balance in the spontaneously hypertensive rat

Spontaneously hypertensive rats (SHR) were given either 'low' (LNa; 0.5 mmol Na 100 g-1 food), 'control' (CNa; 12 mmol) or 'very high' (vHNa; 120 mmol) sodium diets from 5 to 13-14 weeks of age, to explore how these 240-fold variations in Na intake affected body weight, cardiac, renal and adrenal weights, overall water-electrolyte equilibrium and haemodynamic balance during rest, mental stress and blood loss. Body growth was retarded both in vHNa and LNa SHR presumably reflecting disturbed appetite due to the greatly altered dietary Na contents. Compared with CNa SHR, both cardiac and renal weights 100 g-1 body wt were slightly increased in vHNa and decreased in LNa SHR, with opposite changes of adrenal weights. Total body water, haematocrit and plasma Na-K levels were largely equal in the three groups. Furthermore, cardiac output (CO), stroke volume (SV) and central blood volume (CBV) did not differ significantly between groups; if anything, CO and SV were higher and CBV lower in vHNa and LNa SHR than in CNa SHR. However, while mean arterial pressure (MAP) was only marginally elevated in vHNa compared with CNa SHR, both MAP and total peripheral resistance (TPR) were lowered about 15% in LNa SHR with signs of increased sympathetic activity to the heart also during rest. Despite an apparently normal volume and cardiac output balance in LNa SHR, the latter changes suggest a disturbed neuro-hormonal cardiovascular control.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular Responses to Acute Mental ‘Stress' in Spontaneously Hypertensive Rats

Spontaneously hypertensive rats (SHR), aged 7 months (‘manifest’ hypertension) or 10–11 weeks (‘prehypertensive’), and renal hypertensive rats (RHR; ‘nonhereditary’ hypertension were compared with normotensive rats (NCR) concerning cardiovascular responses to mental ‘stress’. Blood pressure and heart rate were followed in pairs of awake SHR—NCR and RHR—NCR, while defence reactions were provoked by alerting stimuli (light, noise, vibrations). The tachycardia, here involving both accentuated sympathetic and centrally suppressed vagal discharge, reflected the intensity of neural activation and the pressuie rise the imposed load on heart and vessels. In both respects the SHR groups responded decidedly stronger than NCR and RHR, also after either adrenergic or vagal cardiac blockade. Since SHR and NCR hearts responded equally to graded vagal stimulations or to isoprenaline, the enhanced tachycardia responses reflected a truly intensified defence reaction in SHR. Further, SHR responded more often to mild stimuli than NCR, suggesting a lower ‘threshold’ for defence reactions, and more frequently with clearcut defence reactions than NCR which exhibited vagal bradycardia responses in 30 %, versus 5 % in SHR. This hyperreactivity and apparent prevalence concerning ‘sympathotonic’ patterns in SHR during alertness, in turn tending to trigger structural vascular adaptation and manifest hypertension, is evidently genetically linked and not secondary to hypertension, being observed particularly in ‘prehypertensive’ SHR but not in RHR.     

Effects of exercise training on pathological cardiac hypertrophy related gene expression and apoptosis

This study determined whether exercise training prevents pathological hypertrophy in the left ventricle by modulation of myocardial and apoptosis-associated genes. We used spontaneously hypertensive rats (n=15, non-exercise SHR), exercise-trained SHR (n=15, treadmill exercise for 12 weeks), and sedentary Wistar-Kyoto (WKY) rats (n=15). Exercise-trained SHR expressed adaptive changes such as reduced body weight, heart rate, blood pressures, left ventricle wall thickness, lipid profiles, and homocysteine level. The mRNA expression of angiotensin converting enzyme, endothelin-1, and brain natriuretic peptides in the heart was lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR, whereas mRNA expression of caveolin-3 and eNOS in the heart was higher. Bcl-2 protein was higher in the exercise-trained SHR than in the WKY and the non-exercise SHR. In contrast, Bax protein levels were lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR. Furthermore, the levels of the active forms of caspase-3 (20 kDa) were lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR. These findings suggest that exercise training prevents pathological hypertrophy in the left ventricle by modulation of myocardial genes and that it interferes with a signal transduction pathway of apoptosis secondary to the pathological cardiac hypertrophy.     

Selective sympathetic neural changes in hypertrophied right ventricle

Selective pressure overload of the right ventricle in guinea pigs resulted in early and sustained reductions in tyrosine hydroxylase and dopamine-beta-hydroxylase activities in the right ventricle. No changes in tyrosine hydroxylase activity were detected in stellate ganglia sinoatrial (SA) nodal region, atrioventricular (AV) nodal region, or left ventricle. Reductions in tyrosine hydroxylase activity in stressed right ventricle were similar regardless of duration of pulmonary artery constriction, extent of hypertrophy, presence or absence of hepatic congestion, and preservation or depletion of catecholamines. The changes may represent localized loss of sympathetic nerve fibers; factors involved directly in the process of pressure-overload-induced hypertrophy may be responsible. However, sympathetic nerves remaining in hypertrophied ventricle respond normally to cold-induced sympathetic activation. The reduction in tyrosine hydroxylase activity and the maintenance of norepinephrine turnover in residual innervation to hypertrophied right ventricle support the concept that sympathetic neural regulation of hypertrophied cardiac tissue is altered but not lost.     

Performance of the hypertrophied left ventricle in spontaneously hypertensive rats. Effects of adrenergic stimulation

The performance of isolated hearts from adult male spontaneously hypertensive rats (SHR) and matched normotensive controls (NCR) was investigated in an antegrade perfusion system, where preload and afterload could be varied independently. During electrical pacing of the heart to constant heart rate, increases in afterload, but not in preload, considerably raised cardiac contractility, measured as left ventricular max dP/dt. At afterloads equalling their respective in vivo ones, max dP/dt was similar in SHR and NCR. This indicates that the SHR hearts by myocardial hypertrophy are so well adapted to their raised afterload that an increased inotropic state of the heart is not required. Upon adrenaline addition, SHR and NCR did not differ concerning either "chronotropic sensitivity", i.e. per cent increase in heart rate of the spontaneously beating heart or in "inotropic sensitivity", measured as increase in max dP/dt. However, in this in vitro situation adrenaline increased stroke volume only when the hearts worked at reduced inotropism, induced by lowered temperature (30 degrees C). At maximal inotropic stimulation by adrenaline and occluded outflow, the SHR hearts produced higher systolic pressures than the NCR ones. This reveals an increased maximal contractile capacity of the hypertrophied SHR left ventricle, rather than a reduced one as sometimes suggested.     

Consequence of Social Isolation on Blood Pressure,Cardiovascular Reactivity and Design in Spontaneously Hypertensive Rats

Spontaneously hypertensive rats (SHR), which inherently display exaggerated cardiovascular defence reactions to environmental stimuli (Hallbäck and Folkow 1974), and normotensive control rats (NCR) were kept isolated after they were weaned to reduce such environmental influences which normally induce psychological activation. Mean arterial pressure was followed until 7 months of age, when the cardiovascular defence reactions to acute mental stress were compared and an analysis of cardiovascular design was made. The isolated SHR but not the isolated NCR, had significantly lower pressures than their unisolated controls. Likewise, judged by the relative weight of the left ventricle and the hemodynamically evaluated design of the hindquarter resistance vessels, the structural cardiovascular adaptation was about proportionally less pronounced in isolated than in control SHR. However, their cardiovascular responses to acute “psychological stress” were equally intense, and clearly exaggerated when compared with NCR. Thus, a prolonged reduction of excitatory environmental influences implies a relatively less pronounced development of hypertension in SHR, even though an inherent hyperreactivity concerning neurohormonal pressor responses to alerting stimuli is present. These findings stress the importance of interacting intrinsic-hereditary and extrinsic neurogenic influences for the initiation of primary hypertension.     

Lipid peroxidation and myocardial vulnerability in hypertrophied SHR myocardium.

In a comparison using age-matched Wistar-Kyoto rats (WKY), 16-week-old male spontaneously hypertensive rat (SHR) hearts were examined histologically and biochemically on the first and fourth day after administration of 20 mg/kg doxorubicin in order to examine whether membrane abnormalities in hypertrophied SHR myocardium are caused by lipid peroxidation. Morphological examination of the SHR revealed focal myocytolysis on the first day and severe cardiomyopathy involving diffuse myocytolysis and vacuolar degeneration in the left ventricle on the fourth day. The activity of a membrane-related enzyme, Na+/K(+)-ATPase, was already lower in control SHR than that of control WKY and was lower in both SHR and WKY than in the respective saline groups on the first day after administration, whereas the enzyme activity in the doxorubicin-treated SHR was not significantly different from that of the treated WKY. A thiobarbituric acid-reactant substance, a lipid peroxidation marker, was significantly higher in treated SHR than it was in the treated WKY on the first day. Furthermore, in comparison with WKY, alpha-tocopherol in the left ventricle in SHR was significantly lower on the fourth day after administration. These results show that a proneness to lipid peroxidation in the membrane system is closely associated with severity of doxorubicin-induced cardiomyopathy in SHR and suggests that membrane lipid peroxidation may cause a higher degree of vulnerability in hypertrophied SHR myocardium.     

Renal sympathetic activity in spontaneously hypertensive rats and normotensive controls, as studied by three different methods

Recordings of sympathetic activity from multifibre preparations of renal nerves have produced conflicting results concerning the presence or absence of an increased sympathetic discharge in spontaneously hypertensive rat (SHR) compared to normotensive Wistar-Kyoto rats (WKY). Therefore, recordings of single fibre activity to the kidney were performed in anesthetized SHR and WKY in comparison with multifibre recordings in conscious, undisturbed rats. A new method of estimating sympathetic discharge by analyzing the variability of "cycle activity" in multifibre nerve recordings was also used. The average nerve activity in a great number of cardiac cycles was then expressed in relation (in per cent) to the nerve activity in a small number of cardiac cycles with the highest and lowest nerve activity in each rat. Single fibre recordings showed a significantly higher sympathetic activity to the kidneys in SHR (3.8 +/- 0.3 Hz) than in WKY (1.7 +/- 0.2 Hz; p less than 0.001). Also average "cycle activity" was significantly higher in conscious SHR (34 +/- 1%) than in WKY (26 +/- 2%, p less than 0.01). This was due to the larger number of cardiac cycles in SHR with high sympathetic activity while WKY showed more of "silent" cardiac cycles which lacked nerve impulses. Further, the recordings of rectified multifibre renal nerve activity also showed an elevated sympathetic activity in conscious SHR rats. The increased renal sympathetic activity appears to reflect the "primary" central nervous "hyperreactivity" characterizing SHR hypertension. It is suggested that the increased renal sympathetic activity may be of particular importance for the development of primary hypertension in SHR and perhaps also in man.     

Consequence of social isolation on blood pressure, cardiovascular reactivity and design in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR), which inherently display exaggerated cardiovascular defence reactions to environmental stimuli (Hallb?ck and Folkow 1974), and normotensive control rats (NCR) were kept isolated after they were weaned to reduce such environmental influences which normally induce psychological activation. Mean arterial pressure was followed until 7 months of age, when the cardiovascular defence reactions to acute mental stress were compared and an analysis of cardiovascular design was made. The isolated SHR but no the isolated NCR, had significantly lower pressures than their unisolated controls. Likewise, judged by the relative weight of the left ventricle and the hemodynamically evaluated design of the hindquarter resistance vessels, the structural cardiovascular adaptation was about proportionally less pronounced in isolated than in control SHR. However, their cardiovascular responses to acute "psychological stress" were equally intense, and clearly exaggerated when compared with NCR. Thus, a prolonged reduction of excitatory environmental influences implies a relatively less pronounced development of hypertension in SHR, even though an inherent hyperreactivity concerning neurohormonal pressor responses to alerting stimuli is present. These findings tress the importance of interacting intrinsic-hereditary and extrinsic neurogenic influences for the initiation of primary hypertension.     

短链酰基辅酶A脱氢酶在大鼠生理性和病理性心肌肥大中的作用

 目的：研究短链酰基辅酶A脱氢酶(short-chain acyl-CoA dehydrogenase, SCAD)在大鼠生理性和病理性心肌肥大中的变化,探讨其与心肌肥大之间的关系。方法：以自发性高血压大鼠作为病理性心肌肥大模型,游泳运动训练性大鼠作为生理性心肌肥大模型。检测大鼠的血压、左室重量指数、血清和心肌游离脂肪酸含量、SCAD mRNA、蛋白表达及其酶活性的变化,采用超声心动图观察心脏的结构及功能。结果：与对照组比较,运动组大鼠出现了明显的离心性肥大,心肌收缩功能增强;而高血压组大鼠呈现出明显的向心性肥大,心肌收缩功能减退。与对照组比较,运动组和高血压组大鼠的左室重量指数均明显增高,但两组间比较无显著差异,二者发生了相同程度的心肌肥大。与对照组比较,运动组大鼠左心室SCAD mRNA和蛋白表达均明显上调,酶活性增高,血清和心肌游离脂肪酸含量明显减少;而自发性高血压大鼠左心室SCAD mRNA和蛋白表达均明显下调,酶活性下降,血清和心肌游离脂肪酸含量明显增多。结论：SCAD在生理性和病理性心肌肥大中呈现出不一致的变化趋势,可能作为区别2种不同心肌肥大的分子标志物以及病理性心肌肥大的潜在治疗靶点。     

Left ventricular hypertrophy improves cardiac performance in spontaneously hypertensive rats

Cardiac function was studied in spontaneously breathing, adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). By rapid intravenous blood infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV) was determined while the cardiac nervous control was pharmacologically blocked. Since SV is greatly influenced by the level of afterload (mean arterial pressure, MAP), SV was also determined at increased MAP (constriction of abdominal aorta) and at decreased MAP (vasodilation by hydralazine). At low LVEDP levels, a righward shift of the Frank-Starling relationship was observed in SHR. This rightward shift seems mainly to depend on the increased MAP present in SHR since it was less prominent if MAP was lowered to normotensive levels in SHR. Maximal SV during volume infusion was similar in SHR and WKY, despite a much higher MAP in SHR. When peak SV was instead compared at similar MAP levels for both (either at ‘normotensive’ or ‘hypertensive’ levels) it was always significantly greater in SHR, and was increased largely in proportion to their increased left ventricular weight. This indicates that the left ventricular hypertrophy present in SHR is, at least at this stage, a physiological adaptation of the heart to increase its performance, in order to maintain a normal SV and hence cardiac output, despite an increased arterial pressure.     

An anomalous case of the thoracic cardiac nerve in the Japanese monkey

A rare case of an anomalous right thoracic cardiac nerve that directly distributed to the left ventricle and left coronary artery was observed in a Japanese monkey. Its nerve arose from 4th and 5th thoracic ganglia on the right sympathetic trunk, descended obliquely along the thoracic vertebra toward the thoracic aorta at the level of the body of 7th thoracic vertebra. After reaching the aorta, it reflected upward and ascended along the medial-ventral surface of the aorta. Thereafter, it received a cardiac branch arising from the vagus nerve in the upper part of the thoracic aorta, and ran to the left-lateral aspect of the heart. Finally, it gave off main branches to the terminal part of the left coronary artery and the left ventricle, and small branches to the proximal part of the left coronary artery. In a human dissection, similar nerves (the thoracic splanchnic nerve or thoracic pulmonary nerve) originating at the thoracic ganglia and reaching to the lung, have also been observed. The superior, middle and inferior cervical cardiac nerves can easily reach the heart along the common carotid artery, the brachiocephalic artery and subclavian artery. But it is not easy for the thoracic cardiac nerve to reach the heart because of the topographical relationship of its thoracic origin and the peripheral distributions of the left side of the heart. Therefore, the thoracic cardiac nerve would have to run a complicated course.     

Differential haemodynamic effects of atrial natriuretic peptide (ANP) in normotensive and spontaneously hypertensive rats

Central haemodynamic parameters and cardiac performance were measured in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) control rats after a 10-min infusion of rat ANP (103-125), 1 micrograms kg-1 min-1. Mean Arterial blood pressure (MAP) decreased by approximately 10% in both groups of rats. Heart rate (HR) increased slightly in both strains during the infusion. In the normotensive group the fall in MAP was due to a reduction in cardiac output (CO) while in the SHR there was a decrease in CO as well as in total peripheral resistance (TPR). The ANP infusion also reduced central blood volume (CBV) and stroke volume (SV) in both groups of rats. The reduction in CBV and CO was significantly more pronounced in the WKY strain. Left ventricular end diastolic pressure (LVEDP) and cardiac contractility (dP/dt) did not change while central venous pressure (CVP) was slightly decreased in the WKY group as a result of the ANP infusion. We conclude that ANP reduces MAP in normotensive animals by a reduction in CO. In the SHR a reduction in TPR also contributes to the fall in MAP. Atrial natriuretic peptide did not exert any negative inotropic effects, but the reduction of CO was due to an increased venous compliance.     

Renal vascular resistance and reactivity in the spontaneously hypertensive rat.

Renal vascular resistance is elevated in spontaneously hypertensive rats (SHR) when compared to normotensive control Wistar-Kyoto rats (WKY). The present study examined possible determinants of this raised vascular resistance in in situ autoperfused kidneys of pentobarbital-anesthetized, 12- to 16-wk-old SHR and WKY. Over a wide range of arterial pressures (30--100 mmHg) renal blood flow was consistently higher in WKY than in SHR. This relative flow difference was unchanged by acute renal denervation, with renal vascular resistance decreasing approximately 20% in both strains. Changes in renal vascular resistance to renal nerve stimulation and the administration of intra-arterial vasoactive hormones also were assessed. Vascular responses to renal nerve stimulation, tyramine, angiotensin II, and acetylcholine were similar in kidneys of the two strains, but reactivity to norepinephrine was significantly less in kidneys of SHR. It was concluded that elevated renal vascular resistance in the SHR does not result from an excessive neurogenic influence on the renal vasculature or from vascular hyperreactivity to norepinephrine or angiotensin II.     

Left atrial pressure in normotensive and spontaneously hypertensive rats

The left atrial pressure in adult spontaneously hypertensive rats (SHR) of the Okamoto strain and normotensive control rat (NCR) was measured via chronically implanted catheters. In SHR left atrial pressure in end-expiration was more than twice as high (10.3±0.4 mmHg) as in NCR (4.6±0.3 mmHg). There was no difference in the intrapleural pressure between the two groups of rats, therefore the enhanced left atrial pressure in SHR represents a real rise in the diastolic filling pressure of its left ventricle. This is considered to be the most important compensation for the earlier reported rightward shift of the Frank-Starling curve in SHR (Hallbäck, Isaksson & Noresson 1975, Noresson et al. 1979a). Without this compensation the stroke volume would have been drastically reduced for the hypertrophied heart.