Mechanism of Pressor Effects of Intraventricular Injection of Angiotensin II in the Rat: Role of Vasopressin and Renal Nerves

1982 ◽  
Vol 63 (3) ◽  
pp. 275-279 ◽  
Author(s):  
Hiromichi Suzuki ◽  
Kazuoki Kondo ◽  
Michiko Handa ◽  
Hiroshi Kawabe ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Intraventricular Injection ◽  
Renal Nerves ◽  
Plasma Vasopressin ◽  
Sympathetic Nervous ◽  
Renal Sympathetic ◽  
Stimulation Of

1. The role of the kidney and vasopressin in the increase of blood pressure obtained when angiotensin II is injected intraventricularly into rats has been investigated. 2. Intraventricular injection of angiotensin II led to a significant increase in blood pressure in the control and all sham-operated rats compared with that in unilaterally nephrectomized, one-kidney denervated rats and bilaterally nephrectomized rats. The degree of increase in blood pressure in unilaterally nephrectomized, one-kidney denervated rats was equal to that in bilaterally nephrectomized rats. 3. The increase in blood pressure in the bilaterally nephrectomized rats lasted significantly longer than that in the control and unilaterally nephrectomized, one-kidney denervated rats. 4. In the bilaterally nephrectomized rats plasma vasopressin was still higher 30 min after the intraventricular injection of angiotensin II than that of the control and unilaterally nephrectomized, one-kidney denervated rats. 5. These results suggest that the rise in blood pressure observed after intraventricular injection of angiotensin II is due partly to stimulation of the renal sympathetic nervous system and partly to increase in plasma vasopressin concentration.

Selective renal medullary damage and hypertension in the rat: The role of vasopressin

1986 ◽  
Vol 71 (2) ◽  
pp. 167-171 ◽  
Author(s):  
G. I. Russell ◽  
N. P. Godfrey ◽  
M. L. Forsling ◽  
R. F. Bing ◽  
H. Thurston ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Response Curve ◽  
Elevated Blood ◽  
Plasma Vasopressin ◽  
Normal Rat ◽  
Sympathetic Nervous

1. The induction of selective renal medullary damage by 2-bromoethylamine hydrobromide (BEA) results in polyuria and raised blood pressure. In view of the likely elevation of plasma vasopressin we have investigated the role of vasopressin (AVP) in the elevated blood pressure in this model. 2. Plasma vasopressin levels in BEA pretreated rats were raised significantly (2 ± 0.6 pg/ml vs 0.8 ± 0.1 in normal rat, P < 0.05) but not to pressor levels. 3. In addition, pressor responsiveness was investigated in renal medullary damaged rats. There was a reduced response to vasopressin and noradrenaline but no alteration with angiotensin II. A specific V1 receptor AVP antagonist [d(CH2)5Tyr(Me)AVP] produced no fall in blood pressure but returned the noradrenaline dose-response curve to normal. This suggests an interaction between vasopressin and the sympathetic nervous system in this model. 4. Thus there is no evidence that vasopressin contributes to the rise in blood pressure produced by chemical renal medullectomy and other mechanisms have to be sought.

Central blood pressure effects of substance P and angiotensin II: Role of the sympathetic nervous system and vasopressin

1981 ◽  
Vol 71 (1) ◽  
pp. 33-42 ◽  
Author(s):  
Thomas Unger ◽  
Wolfgang Rascher ◽  
Christine Schuster ◽  
Ranko Pavlovitch ◽  
Albert Schömig ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Substance P ◽  
Sympathetic Nervous System ◽  
Pressure Effects ◽  
Central Blood Pressure ◽  
Blood Pressure Effects ◽  
Sympathetic Nervous

Activation of renal mechanoreceptors increases vasopressin release in rabbits

1991 ◽  
Vol 261 (2) ◽  
pp. R484-R490 ◽  
Author(s):  
A. Yamamoto ◽  
L. C. Keil ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Renal Pelvis ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Renal Nerves ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Pelvic Pressure ◽  
Stimulation Of

Electrical stimulation of afferent renal nerves increases plasma vasopressin (AVP) concentration, but the role of these nerves in the control of AVP release is not known. The aim of the present study was to investigate the effect of activation of renal mechanoreceptors and chemoreceptors on plasma AVP concentration in anesthetized rabbits. Intrapelvic pressure was increased to activate renal mechanoreceptors, and the renal pelvis was perfused with 1.0 M NaCl, 0.1 M KCl, and 1.0 M mannitol solutions to activate R2 chemoreceptors. With increased pelvic pressure, plasma AVP concentration increased from 12.4 +/- 3.8 to 36.2 +/- 16.1 pg/ml at 5 min and to 37.4 +/- 16.1 pg/ml at 10 min (P less than 0.01). Plasma renin activity increased from 15.7 +/- 4.0 to 22.1 +/- 3.3 ng.ml-1.2 h-1 (P less than 0.05), but blood pressure and heart rate did not change significantly. Similar increases in plasma AVP concentration occurred during perfusion of the renal pelvis with 1.0 M NaCl (17.6 +/- 8.1 to 53.7 +/- 24.0 pg/ml), 0.1 M KCl (9.2 +/- 2.1 to 39.7 +/- 17.3 pg/ml), and 1.0 M mannitol (27.5 +/- 10.9 to 77.5 +/- 30.8 pg/ml) solutions. However, because pelvic pressure increased by 40-50 mmHg during the perfusions, the experiments were repeated with use of a different perfusion method in which pelvic pressure increased by less than 5 mmHg. Under these conditions, plasma AVP concentration did not change significantly during perfusion with any of the solutions. To determine whether the mechanoreceptor-induced increase in AVP release is mediated by the renal nerves, pelvic pressure was increased in another group of rabbits after renal denervation.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of Autonomic Nervous System in Maintenance of Cerebral and Renal Hypertension

1957 ◽  
Vol 188 (2) ◽  
pp. 371-374 ◽  
Author(s):  
Sol Rothman ◽  
Douglas R. Drury
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Renal Hypertension ◽  
The Other ◽  
Peripheral Vasculature ◽  
Blood Pressures ◽  
Sympathetic Nervous ◽  
Blood Pressure Responses

The blood pressure responses to various drugs were investigated in renal hypertensive, cerebral hypertensive and normotensive rabbits. Hexamethonium bromide and Dibenamine reduced the blood pressures of renal and cerebral hypertensives. Effects in the normal were insignificant. The cerebral hypertensive's blood pressure was slightly affected by benzodioxane. Blood pressure was not reduced at all in the other groups. Blood pressure of the renal hypertensive rabbit was greatly reduced by Veriloid and dihydroergocornine. Blood pressures of cerebral and normal animals were affected to a lesser degree. The results suggest that maintenance of hypertension in the cerebral hypertensive rabbit depends on an overactive sympathetic nervous system, possibly due to the release of medullary pressor centers from inhibitory impulses originating in higher centers; whereas, the maintenance of hypertension in the renal hypertensive rabbit may be attributed to an increased reactivity of the peripheral vasculature to a normal sympathetic tone.

Renal denervation alters cardiovascular and endocrine responses to hemorrhage in conscious newborn lambs

1998 ◽  
Vol 275 (1) ◽  
pp. H285-H291 ◽  
Author(s):  
Francine G. Smith ◽  
Isam Abu-Amarah
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Elevated Plasma ◽  
Baseline Levels ◽  
Renal Sympathetic

To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 ± 16 to 207 ± 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 ± 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 ± 6.4 ng ANG I ⋅ ml−1 ⋅ h−1) compared with intact lambs (4.0 ± 1.1 ng ANG I ⋅ ml−1 ⋅ h−1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 ± 8 to 197 ± 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 ± 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.

scholarly journals Role of Sympathetic Nervous System in Cyclosporine-Induced Rise in Blood Pressure

Hypertension ◽  
1999 ◽  
Vol 34 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Mario J. Carvalho ◽  
Anton H. van den Meiracker ◽  
Frans Boomsma ◽  
Joao Freitas ◽  
Arie J. Man in ‘t Veld ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous

Role of the sympathetic nervous system in CCl4 hepatotoxicity

1960 ◽  
Vol 198 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Deane N. Calvert ◽  
Theodore M. Brody
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Liver Mitochondria ◽  
Central Vein ◽  
Fat Depots ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking ◽  
Stimulation Of

An hypothesis is proposed which states that the characteristic hepatic changes seen after the administration of carbon tetrachloride are the result of stimulation of central sympathetic areas which produce a massive discharge of the peripheral sympathetic nervous system. Stimulation of the sympathetic supply to the blood vessels of the liver results in restriction of blood flow in the liver, leading to anoxia and the characteristic necrosis around the central vein of the hepatic lobule. Similarly the discharge causes the release of unesterified fatty acids from the peripheral fat depots and the consequent deposition of lipid in the liver. This hypothesis is based upon experimental evidence using the following physiologic and pharmacologic maneuvers: adrenergic blocking agents, pretreatment with reserpine, adrenalectomy and section of the spinal cord—all are effective to a greater or lesser extent in preventing the changes characteristically seen in oxidative phosphorylation of the liver mitochondria, activation of a Mg-dependent ATPase and deposition of lipid in the liver. Transection of the spinal cord is the most effective treatment and prevents entirely the characteristic changes seen in the above-mentioned functions.

scholarly journals Roles for the sympathetic nervous system, renal nerves, and CNS melanocortin-4 receptor in the elevated blood pressure in hyperandrogenemic female rats

2015 ◽  
Vol 308 (8) ◽  
pp. R708-R713 ◽  
Author(s):  
Rodrigo Maranon ◽  
Roberta Lima ◽  
Frank T. Spradley ◽  
Jussara M. do Carmo ◽  
Howei Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Female Rats ◽  
Elevated Blood Pressure ◽  
Renal Nerves ◽  
Female Rat ◽  
Elevated Blood ◽  
Melanocortin 4 Receptor ◽  
Sympathetic Nervous

Women with polycystic ovary syndrome (PCOS) have hyperandrogenemia and increased prevalence of risk factors for cardiovascular disease, including elevated blood pressure. We recently characterized a hyperandrogenemic female rat (HAF) model of PCOS [chronic dihydrotestosterone (DHT) beginning at 4 wk of age] that exhibits similar characteristics as women with PCOS. In the present studies we tested the hypotheses that the elevated blood pressure in HAF rats is mediated in part by sympathetic activation, renal nerves, and melanocortin-4 receptor (MC4R) activation. Adrenergic blockade with terazosin and propranolol or renal denervation reduced mean arterial pressure (MAP by telemetry) in HAF rats but not controls. Hypothalamic MC4R expression was higher in HAF rats than controls, and central nervous system MC4R antagonism with SHU-9119 (1 nmol/h icv) reduced MAP in HAF rats. Taking a genetic approach, MC4R null and wild-type (WT) female rats were treated with DHT or placebo from 5 to 16 wk of age. MC4R null rats were obese and had higher MAP than WT control rats, and while DHT increased MAP in WT controls, DHT failed to further increase MAP in MC4R null rats. These data suggest that increases in MAP with chronic hyperandrogenemia in female rats are due, in part, to activation of the sympathetic nervous system, renal nerves, and MC4R and may provide novel insights into the mechanisms responsible for hypertension in women with hyperandrogenemia such as PCOS.

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