脑室注射Intermedin1-53对大鼠血压和心率的调节作用

目的探讨Intermedin1-53对正常大鼠中枢神经调节的心血管效应及其可能的机制.方法将药物微量注射入麻醉大鼠侧脑室,观察注药后45 min内血压和心率的变化.结果侧脑室注射不同剂量的Intermedin1-53后可引起血压升高和心率加快,并存在剂量和时间依赖关系.中枢注射Intermedin1-53引起的升高血压的作用明显强于肾上腺髓质素,但其增加心率的作用弱于肾上腺髓质素.Intermedin1-53升高血压和加快心率的作用,可被预先侧脑室注射肾上腺髓质素受体拮抗剂ADM22-52以及prepro-IMD抗血清阻断.结论本工作提示Intermedin1-53是调节血压和心率的一个重要的中枢活性因子.     

侧脑室内注射血管紧张素-(1-7)对大鼠心血管活动的调节作用

目的 探讨脑室内外源性血管紧张素-(1-7)[angiotensin-(1-7),Ang-(1-7)]对正常大鼠心血管活动的影响.方法 雄性Wistar大鼠24只,随机分为Ang-(1-7)小剂量(2.5 μg)组、中剂量(10 μg)组、大剂量(26 μg)组1 d对照组(生理盐水),每组6只.观察注药前后大鼠血压和心率的变化.结果 Ang-(1-7)注入Wistar 大鼠侧脑室后引起血压升高和心率增快,与对照组比较差异显著(P＜0.05,P＜0.01).Ang-(1-7)中剂量组变化最明显.结论 在侧脑室可能存在Ang-(1-7)的特异性受体,并且提示Ang-(1-7)是调节血压和心率的一个重要中枢活性因子.     

外周给予肾上腺髓质素对大鼠血糖和血糖调节激素的影响

外周给予肾上腺髓质素对大鼠血糖和血糖调节激素的影响齐红伟，赵咏梅，刘月琴，盛树力肾上腺髓质素（ａｄｒｅｎｏｍｅｄｕｌｌｉｎ，ＡＭ）是从肾上腺髓质嗜铬细胞中发现的５２肽，具有扩张血管、减少外周循环阻力、降低血压的作用。而扩张血管最有效的降钙素基因相关肽...     

肾上腺髓质素与肺动脉高压

肾上腺髓质素是一种新发现的降压肽，广泛分布于体内多种脏器具有调节动脉血压、细胞增殖等作用。肺脏是肾上腺南素生成和代谢的重要器官。肺动脉高压时血清中肾上腺髓质纱深度明显升高，其ｍＲＮＡ在右心室表达啬外源性的肾上腺髓质素能扩张在体和离体的肺动脉，降低肺动脉压，啬肺血流量，认为肾上腺髓质素在肺动脉高压的代偿机制中起重要作用，并有望用于治疗肺动脉高压。     

肾上腺髓质素与肺动脉高压

肾上腺髓质素是一种新发现的降压肽,广泛分布于体内多种脏器,具有调节动脉血压、细胞增殖等作用。肺脏是肾上腺髓质素生成和代谢的重要器官。肺动脉高压时血清中肾上腺髓质素浓度明显升高,其mRNA在右心室表达增加,外源性的肾上腺髓质素能扩张在体和离体的肺动脉,降低肺动脉压,增加肺血流量,认为肾上腺髓质素在肺动脉高压的代偿机制中起重要作用,并有望用于治疗肺动脉高压。     

瘦素通过下丘脑室旁核、腹内侧核及背内侧核调节血压

目的 研究室旁核(PVN)、腹内侧核(VMH)及背内侧核(DMH)微注射瘦素对血压(BP)的调节作用,揭示瘦素BP调节的可能中枢位点.方法 以SD大鼠为研究对象,采用脑立体定位脉冲电刺激及核团内微注射瘦素的方法,观察PVN、VMH及DMH在瘦素BP调节中的作用,同时收集大鼠尿液进行尿量(UV)及尿电解质分析.结果 PVN、VMH、DMH微注射瘦素后,均可引起明显的BP升高、心率(HR)加快等BP调节反应:PVN内注射瘦素后,BP较注射前升高(16.3±5.0)mm Hg,心率增加(57.7±15.2)次/min;VMH微注射瘦素后,BP较前升高(11.5±2.6)mm Hg,心率增加(39.8±3.2)次/min;DMH微注射瘦素后,BP较前升高(13.1±1.5)mm Hg,心率增加(51.9±19.2)次/min,与各自的对照组相比,上述改变均具有统计学意义.然而,与脉冲电刺激产生的即刻、短期升压效应不同,瘦素的升压作用出现较慢但持续时间长,大约在注射后20～30 min达到高峰,持续到试验结束尚不能完全恢复到干预前水平,同时伴UV和尿钠(Una)排泄减少的趋势.结论 瘦素作用于中枢神经系统可引起BP升高、HR加快等心血管反应,PVN、VMH、DMH可能是瘦素引起BP升高的中枢作用位点,并且推测这些核团可能是肥胖性高血压发病中枢机制中的重要环节.     

瘦素通过下丘脑室旁核、腹内侧核及背内侧核调节血压

目的研究室旁核(PVN)、腹内侧核(VMH)及背内侧核(DMH)微注射瘦素对血压(BP)的调节作用,揭示瘦素BP调节的可能中枢位点。方法以SD大鼠为研究对象,采用脑立体定位脉冲电刺激及核团内微注射瘦素的方法,观察PVN、VMH及DMH在瘦素BP调节中的作用,同时收集大鼠尿液进行尿量(UV)及尿电解质分析。结果PVN、VMH、DMH微注射瘦素后,均可引起明显的BP升高、心率(HR)加快等BP调节反应PVN内注射瘦素后,BP较注射前升高(16·3±5·0)mmHg,心率增加(57·7±15·2)次/min;VMH微注射瘦素后,BP较前升高(11·5±2·6)mmHg,心率增加(39·8±3·2)次/min;DMH微注射瘦素后,BP较前升高(13·1±1·5)mmHg,心率增加(51·9±19·2)次/min,与各自的对照组相比,上述改变均具有统计学意义。然而,与脉冲电刺激产生的即刻、短期升压效应不同,瘦素的升压作用出现较慢但持续时间长,大约在注射后20~30min达到高峰,持续到试验结束尚不能完全恢复到干预前水平,同时伴UV和尿钠(UNa)排泄减少的趋势。结论瘦素作用于中枢神经系统可引起BP升高、HR加快等心血管反应,PVN、VMH、DMH可能是瘦素引起BP升高的中枢作用位点,并且推测这些核团可能是肥胖性高血压发病中枢机制中的重要环节。     

下丘脑内血管升压素在紧张应激引起大鼠血压升高反应中的作用

目的观察下丘脑血管升压素（ｖａｓｏｐｒｅｓｓｉｎ，ＡＶＰ）在慢性紧张应激引起大鼠血压升高过程中的作用。方法实验在给予慢性应激刺激后，引起动物血压出现显著升高的雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠中进行。在通过侧脑室（ｉｃｖ．）及外周静脉（ｉｖ．）给予大鼠注射血管升压素Ｖ１受体拮抗剂ｄ（ＣＨ２）５Ｔｙｒ（Ｍｅ）ＡＶＰ后，观察其对动物平均动脉压（ＭＢＰ）的影响。结果在正常大鼠中ｉｃｖ．或ｉｖ．注射ｄ（ＣＨ２）５Ｔｙｒ（Ｍｅ）ＡＶＰ后，动物ＭＢＰ无显著改变，但在慢性应激引起血压出现显著升高的大鼠中，ｉｃｖ．ｄ（ＣＨ２）５Ｔｙｒ（Ｍｅ）ＡＶＰ后，动物血压出现显著降低，降压反应持续约２ｈ，最大效应出现在给药后约４５ｍｉｎ，大鼠ＭＢＰ从给药前的１３４±１１．９ｍｍＨｇ的基础上，平均下降３５．６±１２．６ｍｍＨｇ，而通过ｉｖ．ｄ（ＣＨ２）５Ｔｙｒ（Ｍｅ）ＡＶＰ后，却未观察到ＭＢＰ有显著改变。结论由下丘脑合成并释放的ＡＶＰ参与慢性应激引起的大鼠血压升高反应，其作用可能主要通过中枢Ｖ１受体实现     

PAMP增强肾上腺素和去甲肾上腺素升血糖的作用

我们在研究肾上腺髓质素前体Ｎ端２０肽（ＰＡＭＰ）时，发现应用ＰＡＭＰ剂量在３０．０ｎｍｏｌ／ｋｇ时可引起大鼠心律失常发生率高达６４．７％。在５ｎｍｏｌ／ｋｇ时可明显增强肾上腺素（Ｅ）和去甲肾上腺素（ＮＥ）的致心律失常作用（未发表资料），而Ｅ也是升高血...     

下丘脑内血管升压素在紧张应激引起大鼠血压高反应中的作用

目的 观察下丘脑血管升压素（ｖａｓｏｐｒｅｓｓｉｎ，ＡＶＰ）在慢性紧张应激引起大鼠血压升高过程中的作用。方法 实验在给予慢性应激刺激后，引起动物血压出现显著升高的雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠中进行。在通过侧脑室（ｉｃｖ．）及外周静脉（ｉｖ．）给予大鼠注射血管升压素Ｖ１受体拮抗剂ｄ（ＣＨ２）５Ｔｙｒ（Ｍｅ）ＡＶＰ后，观察其支动物平均动脉压（ＭＢＰ）的影响。结果 在正常大鼠中ｉｃｖ．或ｉｖ．注     

Central cardiovascular action of urotensin II in conscious rats

OBJECTIVE: To examine the central cardiovascular action of urotensin II in conscious rats. METHODS: Intracerebroventricular (ICV) injections of urotensin II (1 and 10 nmol) were carried out in conscious Wistar rats. The effects of intravenous (i.v.) urotensin II (10 nmol) were also determined. RESULTS: The ICV injection of urotensin II at a dose of 1 nmol did not alter the arterial pressure or heart rate significantly, while 10 nmol urotensin II increased the arterial pressure and heart rate. The mean arterial pressure at 5 min of ICV urotensin II was 121 +/- 4 mmHg, which was significantly higher than that obtained by ICV injection of artificial cerebrospinal fluid (107 +/- 3 mmHg, P <0.05). In addition, significant increases in heart rate were observed 5-15 min after ICV urotensin II. Pre-treatment with pentolinium (5 mg/kg, i.v.) significantly attenuated the increases in mean arterial pressure (20 +/- 3 versus 8 +/- 2 mmHg, P <0.01) and heart rate (78 +/- 18 versus 7 +/- 5 beats/min, P <0.05) induced by ICV urotensin II. On the other hand, i.v. injection of urotensin II (10 nmol) elicited a depressor response associated with tachycardia; mean arterial pressure 5 min after injection was significantly lower in the urotensin II-injected rats (89 +/- 5 mmHg) than in the control rats (102 +/- 2 mmHg, P <0.05), and the heart rate was significantly higher in the former (402 +/- 11 versus 360 +/- 9 beats/min, respectively, P <0.05). CONCLUSIONS: Central urotensin II produces pressor and tachycardic responses through sympathetic activation, while peripheral urotensin II exerts a vasodilation-mediated depressor response in conscious rats.     

Central adrenomedullin augments the baroreceptor reflex in conscious rabbits

We examined the roles of central adrenomedullin, proadrenomedullin N-terminal 20 peptide (PAMP), and calcitonin gene-related peptide (CGRP) on the baroreceptor reflex in conscious rabbits. Intracerebroventricular injection of adrenomedullin (0.2 and 1 nmol/80 microL) elicited dose-related increases in arterial pressure and renal sympathetic nerve activity. On the other hand, a subpressor dose of intracerebroventricular infusion of adrenomedullin (1 nmol/300 microL per hour) caused significant increases in baroreflex sensitivities assessed by renal sympathetic nerve activity and heart rate compared with vehicle infusion (Gmax; -14.9+/-1.7 versus -8.0+/-0.7%/mm Hg, P<0.01, and -8.1+/-0.8 versus -5.1+/-0.5 bpm/mm Hg, P<0.01, respectively). Intracerebroventricular infusion of CGRP (1 nmol/300 microL per hour), which is structurally homologous to adrenomedullin, also enhanced the baroreflex controls of renal sympathetic nerve activity and heart rate. However, the intracerebroventricular infusion of PAMP (30 nmol/300 microL per hour) failed to alter the baseline levels of arterial pressure and baroreflex sensitivities. These results suggest that central adrenomedullin and CGRP, but not PAMP, participate in cardiovascular regulation to augment the baroreflex controls of renal sympathetic nerve activity and heart rate in conscious rabbits.     

Hypotension and hypothalamic depression produced by intracerebroventricular injections of GABA in spontaneously hypertensive rats

To determine the central effects of 4-Amino-n-butyric acid (GABA), pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were recorded following the intracerebroventricular (ICV) injection of GABA. In normotensive Wistar rats, anesthetized with urethane, ICV injections of GABA (50-200 micrograms) reduced sympathetic nerve activity, arterial blood pressure, and heart rate in a dose-dependent manner. Graded electrical stimulation of the ventromedial hypothalamus (50, 100, 150 microA) increased not only mean blood pressure but also the rate of sympathetic nerve firing, and both responses were attenuated by GABA pretreatment (100, 200 micrograms, ICV). In spontaneously hypertensive rats (SHR), ICV-injected GABA also reduced sympathetic and cardiovascular activity, but the magnitude of depressor responses was significantly larger in SHR than in normotensive Wister Kyoto controls (WKY). Pressor and sympathetic nerve responses elicited by ventromedial hypothalamic stimulation were initially larger in SHR than in WKY, but upon subsequent ICV injection of GABA, hypothalamic responsiveness in SHR was inhibited more prominently and became comparable to that in WKY. These results suggest that by depressing hypothalamic function, centrally injected GABA decreases sympathetic nerve activity to thereby lower blood pressure and heart rate, and in SHR, ICV-injected GABA reversed hypothalamo-sympathetic hyperactivity and thus attenuated hypertension.     

Intracerebroventricular injections of endothelin increase arterial pressure in conscious rats

We investigated the possible effects of endothelin (ET) on the central regulation of arterial pressure by injecting ET intracerebroventricularly (ICV) into conscious rats. ICV injections of ET caused dose-dependent elevation of arterial pressure and increase of heart rate. The first reaction was abolished by bunazosin, an alpha 1-adrenergic blocker, injected intravenously. However, the increase in arterial pressure and heart rate caused the rats, injected with ET ICV, to roll to the left on their long axis for 20-30 min, followed by prolonged sedation. Furthermore, the pressor responses and tachycardia were significantly attenuated by the ICV pretreatment with nicardipine, a calcium channel blocker, and nicorandil, a nitrate derivative, respectively. These results suggest that ET may elevate the intracellular Ca2+ concentration ([Ca2+]i) of sympathetic nerve activity regulatory neurons of the brain, leading to an accelerated outflow of sympathetic nerve activity and cause the elevation of arterial pressure.     

Central hypotensive action of clonidine requires nitric oxide

Background- Clonidine has an antihypertensive effect by its action in the brain and, because we observed that the tonic production of nitric oxide (NO) in the brain is required to maintain blood pressure at its low, normotensive level, the current study was designed to determine whether the hypotensive action of clonidine resulted from its stimulation of excess NO in the brain. Methods and Results- Porphyritic microsensors were used to quantify NO concentration in the nucleus tractus solitarius (NTS) in vitro in brain slices and in vivo in the anesthetized rat. In both preparations, the basal production of NO in the NTS was 15+/-3 nmol/L. In vitro stimulation of the NTS with clonidine (50 nmol/L) resulted in an increase in the NO concentration to 84+/-7 nmol/L. In vivo, the intracerebroventricular (ICV) infusion of clonidine (0.03 microgram) caused an increase in NO concentration in the NTS to 128+/-17 nmol/L. This ICV injection of clonidine caused a fall in mean arterial pressure of -22+/-1 mm Hg and a decrease of heart rate of -18+/-2%. The blockade of NO production with N(G)-nitro-L-arginine-methyl ester (2 micromol; delivered ICV, 30 minutes before the clonidine) reduced responses to clonidine for both mean arterial pressure and heart rate (-3+/-1 mm Hg and -2+/-1% change, respectively). Conclusion- The stimulation of the release of NO in the brain by clonidine contributes to its central antihypertensive action.     

Effects of nicardipine on the systemic and renal hemodynamics in acutely elevated blood pressure induced by vasoactive agents in conscious rabbits

The effects of the calcium antagonist, nicardipine, on blood pressure and renal hemodynamics were examined in rabbits with norepinephrine- and angiotensin II-induced elevation of blood pressure. With norepinephrine-infusion, the mean arterial pressure increased from 84 +/- 4 to 118 +/- 4 mmHg accompanied by decreases in heart rate (10%) and renal blood flow (45%). In contrast to the changes in renal blood flow with norepinephrine-infusion, renal blood flow following angiotensin II-induced elevation of blood pressure was decreased by more than 60% at the same degree of elevation of mean arterial pressure. Both intravenous and intrarenal administration of nicardipine (1 microgram/kg) reduced the mean arterial pressure and restored the decreased heart rate and renal blood flow in both norepinephrine- and angiotensin II-infused animals. Intrarenal injection of nicardipine decreased the elevated mean arterial pressure of angiotensin II-induced hypertension more than did intravenous injection (16 +/- 2 vs. 11 +/- 3 mmHg, p less than 0.05). Renal nerve denervation did not lead to any significant effects on the mean arterial pressure, heart rate and renal blood flow following intravenous or intrarenal injection of nicardipine in norepinephrine-infused animals. On the other hand, in angiotensin II-induced elevation of blood pressure, the potentiated hypotensive effect of intrarenal injection of nicardipine was lost in renally denervated animals. In conclusion, the calcium antagonist, nicardipine, was shown to reduce the acutely elevated blood pressure caused by norepinephrine or angiotensin II. In angiotensin II-induced elevation of blood pressure, the renal vasculature may play a more important role in both pressor and depressor aspects in the regulation of blood pressure as compared to its role in norepinephrine-induced hypertension.     

Salt-induced hypertension in a mouse model of liddle syndrome is mediated by epithelial sodium channels in the brain

Neural precursor cell expressed and developmentally downregulated 4-2 protein (Nedd4-2) facilitates the endocytosis of epithelial Na channels (ENaCs). Both mice and humans with a loss of regulation of ENaC by Nedd4-2 have salt-induced hypertension. ENaC is also expressed in the brain, where it is critical for hypertension on a high-salt diet in salt-sensitive rats. In the present studies we assessed whether Nedd4-2 knockout (-/-) mice have the following: (1) increased brain ENaC; (2) elevated cerebrospinal fluid (CSF) sodium on a high-salt diet; and (3) enhanced pressor responses to CSF sodium and hypertension on a high-salt diet, both mediated by brain ENaC. Prominent choroid plexus and neuronal ENaC staining was present in -/- but not in wild-type mice. In chronically instrumented mice, ICV infusion of Na-rich artificial CSF increased mean arterial pressure 3-fold higher in -/- than in wild-type mice. ICV infusion of the ENaC blocker benzamil abolished this enhancement. In telemetered -/- mice on a high-salt diet (8% NaCl), CSF [Na(+)], mean arterial pressure, and heart rate increased significantly, mean arterial pressure by 30 to 35 mmHg. These mean arterial pressure and heart rate responses were largely prevented by ICV benzamil but only to a minor extent by SC benzamil at the ICV rate. We conclude that increased ENaC expression in the brain of Nedd4-2 -/- mice mediates their hypertensive response to a high-salt diet by causing increased sodium levels in the CSF, as well as hyperresponsiveness to CSF sodium. These findings highlight the possible causative contribution of central nervous system ENaC in the etiology of salt-induced hypertension.     

Hypotensive and natriuretic actions of adrenomedullin in subjects with chronic renal impairment

Plasma levels of adrenomedullin are increased in chronic renal failure. The significance of this finding is uncertain, because the biological effects of adrenomedullin in renal impairment are unknown. Therefore, we studied the effects of adrenomedullin infusion in subjects with chronic renal impairment. Eight males with IgA nephropathy and plasma creatinine of 0.19+/-0.03 mmol/L (mean+/-SEM) were studied in a vehicle-controlled crossover design. Each subject was studied twice; subjects were administered either adrenomedullin at a low dose and then a high dose (2.9 and 5.8 pmol/kg per minute, respectively, for 2 hours each) or a 4-hour vehicle control (Hemaccel), in random order, on day 4 of controlled metabolic diets. Adrenomedullin infusion achieved plasma adrenomedullin concentrations in the pathophysiological range after the low (31.2+/-5.1 pmol/L) and high (47.4+/-4.3 pmol/L) dose, and plasma cAMP was increased. Compared with vehicle control, high-dose adrenomedullin increased peak heart rate (+21.7+/-3.3 bpm, P<0.01) and cardiac output (+2.9+/-0.2 L/min, P<0.01) and lowered both systolic and diastolic blood pressures by >10 mm Hg (P<0.05). Plasma renin activity, angiotensin II, and norepinephrine increased by up to 50% above baseline levels (P<0.05 for all), whereas aldosterone and epinephrine were unchanged. Urinary volume and sodium excretion increased significantly (P<0.05) with low-dose adrenomedullin, whereas creatinine clearance was stable, and proteinuria tended to decrease. In subjects with chronic renal impairment due to IgA nephropathy, adrenomedullin infusion lowered blood pressure, stimulated sympathetic activity and renin release, and caused diuresis and natriuresis. Adrenomedullin may have a role in modulating blood pressure and kidney function in renal disease.     

Central cardiovascular action of urotensin II in spontaneously hypertensive rats.

We have previously reported that urotensin II acts on the central nervous system to increase blood pressure in normotensive rats. In the present study, we have determined the central cardiovascular action of urotensin II in spontaneously hypertensive rats (SHR). Intracerebroventricular (ICV) injection of urotensin II elicited a dose-dependent increase in blood pressure in both SHR and normotensive Wistar-Kyoto rats (WKY). The changes in mean arterial pressure induced by ICV urotensin II at doses of 1 and 10 nmol in the WKY were 8 +/- 2 and 23 +/- 3 mmHg, respectively. ICV administration of urotensin II caused significantly greater increases in blood pressure in SHR (16 +/- 3 mmHg at 1 nmol and 35 +/- 3 mmHg at 10 nmol, respectively) compared with those in WKY. Urotensin II (10 nmol) elicited significant and comparable increases in heart rate in SHR (107 +/- 10 bpm) and WKY (101 +/- 21 bpm). Plasma epinephrine concentrations after ICV administration of 10 nmol urotensin II were 203 +/- 58 pmol/ml in SHR and 227 +/- 47 pmol/ml in WKY, which tended to be higher than those in artificial cerebrospinal fluid-injected rats (73+/- 7 and 87 +/- 28 pmol/ml, respectively, p < 0.1). The immunoreactivity of urotensin II receptor GPR 14 was expressed extensively in the glial cells within the brainstem, hypothalamus, and thalamus. These results suggest that central urotensin II may play a role in the pathogenesis of hypertension in SHR. Since GPR 14 was expressed in the glial cells of the brain, urotensin II may act as a neuromodulator to regulate blood pressure.     

Role of vasopressin in cardiovascular and neurohormonal responses to intracerebroventricular hypertonic NaCl

To determine the significance of vasopressin in cardiovascular and neurohormonal responses caused by centrally administered hypertonic NaCl, we examined the effects of a vasopressin antagonist on blood pressure, heart rate, plasma levels of catecholamines, cortisol and renin activity in anesthetized dogs. Intracerebroventricular (ICV) injections of 0.2 ml of 1.5 M NaCl increased mean arterial blood pressure (+29.7 +/- 3.0 mmHg, mean +/- SE), heart rate (+27.9 +/- 7.0 beats/min), plasma concentrations of vasopressin (+48.9 +/- 8.2 pg/ml), norepinephrine (+40.0 +/- 6.2 pg/ml), epinephrine (+231.4 +/- 21.4 pg/ml) and cortisol (+5.3 +/- 1.1 micrograms/dl) and decreased plasma renin activity (-2.0 +/- 0.4 ng/ml/hr). An intravenous vasopressin antagonist, d(CH2)5Tyr(Me)AVP, at a dose of 10 micrograms/kg, attenuated the pressor response and augmented the heart rate response to ICV 1.5 M NaCl. The vasopressin antagonist also augmented the change in plasma norepinephrine and significantly attenuated the responses of cortisol and renin. Baseline levels of these variables were not altered by the vasopressin antagonist except for an increase in renin activity. Two injections of hypertonic NaCl without any pretreatment produced similar cardiovascular and hormonal responses. These results suggest that vasopressin contributes not only to an increase in blood pressure, but also to changes in the sympathetic nervous system, the hypothalamo-adrenocortical axis and the peripheral renin-angiotensin system in response to a central sodium stimulus.