Role of vasopressin in the control of arterial pressure

1983 ◽  
Vol 61 (11) ◽  
pp. 1226-1235 ◽  
Author(s):  
J. Robert McNeill
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Renin Angiotensin System ◽  
Reflex Activity ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Resistance Vessels ◽  
Autonomic Insufficiency

Elevations in the circulating levels of vasopressin within the physiological range (less than 30 fmol ∙ mL−1) in conscious animals cause vasoconstriction of resistance vessels, the most profound effect occurring in the muscle, skin, and intestinal vascular beds. In the organism with normal baroreceptor function, the vasoconstriction is not expressed as an increase in arterial pressure because of a corresponding fall in cardiac output associated with enhanced cardiovascular reflex activity. When compensatory reflex mechanisms are impaired (baroreceptor-denervated dogs, patients with autonomic insufficiency, hypertensive rats), the vasoconstrictor activity of vasopressin is exposed and is reflected as an increase in arterial pressure. Inactivation of the vasopressin system alone by hypophysectomy or by administration of antagonists of the pressor activity of vasopressin is often accompanied by compensatory activation of the rennin–angiotensin system. Thus, under certain conditions, the vasopressin system and the renin–angiotensin system operate as reciprocal or redundant mechanisms in the control of resistance vessels and of arterial pressure. In two rat models of hypertension (spontaneously hypertensive rats and DOC-salt hypertensive rats) plasma levels of vasopressin are elevated, inactivation of the vasopressin system lowers arterial pressure, and pressor responsiveness to the peptide is enhanced. The enhanced pressor responsiveness appears related in part to impaired reflex activity. The mechanism of the impaired reflexes is unknown but in spontaneously hypertensive rats it might be related to a vasopressin deficit in the paraventricular nucleus and brain stem. The evidence is consistent with the possibility that vasopressin is one factor among many that may play a role in the maintenance of arterial pressure in the adult spontaneously hypertensive rat and in the development and maintenance of the hypertensive state in DOC-salt hypertensive rats.

The persistent effect of long-term enalapril on pressure natriuresis in spontaneously hypertensive rats

1997 ◽  
Vol 273 (1) ◽  
pp. F104-F112 ◽  
Author(s):  
S. A. Dukacz ◽  
M. A. Adams ◽  
R. L. Kline
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Day Treatment ◽  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Persistent Effect ◽  
Pressure Natriuresis

Long-term angiotensin-converting enzyme inhibitor treatment has been shown to have a persistent antihypertensive effect in spontaneously hypertensive rats (SHR) long after discontinuation of treatment. To test the hypothesis that this persistent effect involves a shift in the pressure-natriuresis relation, we performed experiments in male, anesthetized SHR at 18 wk of age with fixed neural and hormonal influences on the kidney. Renal function was assessed at various levels of arterial pressure using standard clearance techniques. Enalapril (25 mg.kg-1.day-1 in drinking water) was administered from 4 to 14 wk of age and again 3 days before renal function studies. The following four groups of SHR were studied: 1) 10-wk treatment, 2) 10-wk + 3-day treatment, 3) 3-day treatment, and 4) untreated. Groups 1 and 4 had an intact renin-angiotensin system; groups 2 and 3 had the renin-angiotensin system blocked. Mean arterial pressure (MAP, mmHg; means +/- SE) under Inactin anesthesia was 139 +/- 4 (n = 9), 109 +/- 3 (n = 8), 149 +/- 1 (n = 9), and 181 +/- 7 mmHg (n = 9) for each of the four groups, respectively. Glomerular filtration rate was similar in all groups at resting levels of MAP, whereas renal blood flow was elevated in all treatment groups when compared with that in untreated SHR. Pressure-natriuresis, pressure-diuresis, and pressure-fractional sodium excretion curves for the 10-wk treatment group and 3-day only treatment group were shifted leftward to significantly lower pressures by approximately 25 mmHg, compared with the untreated group. The curves for the treated +3-day group were shifted an additional 30 mmHg to the left. The relationship between renal artery pressure (RAP) and renal interstitial hydrostatic pressure was also shifted 25-30 mmHg but only in rats that received the long-term treatment with enalapril. Three-day enalapril had no significant effect on this relationship. These data indicate that the persistent effect of long-term enalapril treatment on arterial pressure in SHR is the result of a shift in the pressure-natriuresis relationship. The mechanism for this effect involves hemodynamic changes that act to improve transmission of RAP to the interstitium, resulting in enhanced sodium excretion for a given level of RAP.

Significance of the Brain Renin—Angiotensin System in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 159s-161s ◽  
Author(s):  
Jeroen A. D. M. Tonnaer ◽  
Joke J. van Put ◽  
Victor M. Wiegant ◽  
Wybren de Jong
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Renin Angiotensin System ◽  
Hypotensive Effect ◽  
Sympathetic Outflow ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin ◽  
The Brain

1. The renin inhibitor N-acetyl-pepstatin was infused for 14 days or 5 days into the cerebral ventricular system of young and adult spontaneously hypertensive rats respectively. 2. The blood pressure and heart rate of the young animals was significantly lower as a result of this treatment, whereas the pressure of the adult animals tended to decrease. 3. The mechanism involved in the hypotensive effect of N-acetyl-pepstatin appeared to be independent of the peripheral renin-angiotensin system. The possible involvement of a decreased sympathetic outflow is suggested. 4. The present data indicate that the brain renin-angiotensin system contributes to the development of hypertension in the spontaneously hypertensive rat.

Renin-angiotensin system in stroke-prone spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. H409-H416 ◽  
Author(s):  
M. Shibota ◽  
A. Nagaoka ◽  
A. Shino ◽  
T. Fujita
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.

Clonidine fails to reduce pressor responsiveness of conscious spontaneously hypertensive rats to vasopressin

1986 ◽  
Vol 64 (3) ◽  
pp. 284-289 ◽  
Author(s):  
Sunil Datar ◽  
William H. Laverty ◽  
J. Robert McNeill
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Reflex Activity ◽  
Unexpected Finding ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Shr And Wky Rats

Pressor responses and heart rate responses to intravenous injections (3.5–50.0 pmol/kg) of arginine vasopressin (AVP) were recorded in saline- and clonidine-treated spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Clonidine (20 μg/kg, i. v.) caused a marked fall of arterial pressure in SHR but not in WKY rats so that, 20 min after the injection of the α2-adrenoceptor agonist, arterial pressure was similar in the two strains of rats. The curve expressing the relationship between the dose of AVP and the increase of arterial pressure for saline-treated SHR was positioned to the left of that for saline-treated WKY rats. This enhanced pressor responsiveness of SHR to AVP may have been related to impaired reflex activity since heart rate fell much less in SHR than in WKY rats for a given elevation in pressure. Pressure responses to AVP were augmented by clonidine in both SHR and WKY rats so that, similar to saline-treated rats, pressor responsiveness to the peptide was still greater in SHR. Heart rate responses to AVP were not altered significantly by clonidine. The results indicate that clonidine fails to enhance reflex activity and reduce pressor responsiveness of SHR to AVP. The increased pressor responsiveness of both SHR and WKY rats to AVP following clonidine was an unexpected finding and may be related to a peripheral interaction between α-adrenergic agonists and AVP.

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