Effect of Acute Vasopressin Infusion on Blood Pressure and Plasma Angiotensin II in Normotensive and DOC A—Salt Hypertensive Rats

1982 ◽  
Vol 62 (2) ◽  
pp. 143-149 ◽  
Author(s):  
J. J. Morton ◽  
C. Garcia Del Rio ◽  
Maria J. Hughes
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Concentrations ◽  
Hypertensive Rats ◽  
Short Term ◽  
Response Curves ◽  
Plasma Vasopressin ◽  
Salt Hypertension ◽  
Plasma Angiotensin ◽  
Basal Plasma

1. Arginine vasopressin was infused at 0.5, 2, 6, 18 or 54 ng min−1 kg−1 for 1 h into normal, sham-operated and DOCA—salt hypertensive rats. Complete vasopressin/blood pressure dose—response curves were constructed from circulating plasma vasopressin concentrations measured at the end of each infusion. 2. DOCA—salt hypertensive rats had a higher basal plasma vasopressin concentration (11.1 ± sd 3.7 fmol/ml) than either the normal (3.9 ± 2.3, P < 0.01) or the sham-operated rats (4.5 ± 2.4, P < 0.01). 3. The DOCA—salt hypertensive rats did not have any detectable enhancement of pressor sensitivity, compared with either of the two normotensive groups. 4. There was no significant increase in blood pressure in either the normal rats or sham-operated rats until vasopressin was infused at 2 ng min−1 kg−1, when the plasma concentration was between 30 and 40 fmol/ml. 5. Subpressor infusion of vasopressin in the normal and sham-operated rats, which gave plasma concentrations of 22–23 fmol/ml, completely suppressed plasma angiotensin II to levels similar to the basal values found in the DOCA—salt hypertensive rats (10.5 ± 2.3, 14.5 ± 4.5 and 8.0 ± 1.6 fmol/ml respectively). 6. These findings suggest that the mechanism of vasopressin involvement in DOCA—salt hypertension is as yet unclear, that short-term changes in vasopressin concentration appear unimportant in the regulation of normal blood pressure, that small physiological changes of vasopressin in normal rats may be important in the regulation of renin secretion, and that the increase in vasopressin concentration seen in DOCA—salt hypertension may contribute to the suppression of renin and angiotensin II in this state.

Pressor Responsiveness to Angiotensin in Renovascular and Steroid Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 47s-50s ◽  
Author(s):  
E. S. Marks ◽  
H. Thurston ◽  
R. F. Bing ◽  
J. D. Swales
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Receptor Occupancy ◽  
Bilateral Nephrectomy ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Pressor Responses ◽  
Salt Hypertension ◽  
Converting Enzyme Inhibition

1. The pressor response to angiotensin II was reduced in rats with early (&lt;6 weeks) and chronic (&gt;4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA—salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.

The Response of Blood Pressure to Infusion of Angiotensin II: Relation to Plasma Concentrations of Renin and Angiotensin II

1972 ◽  
Vol 42 (4) ◽  
pp. 489-504 ◽  
Author(s):  
R. H. Chinn ◽  
Gisela Düsterdieck
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Diastolic Pressure ◽  
Pressor Response ◽  
Human Subjects ◽  
Plasma Concentrations ◽  
Negative Relationship ◽  
Straight Line ◽  
Plasma Angiotensin ◽  
Standard Rate

1. In thirty-nine normotensive and hypertensive human subjects plasma concentrations of angiotensin II during pressor infusions of the peptide were significantly related to the concentrations found before infusion began. 2. When mean diastolic pressure before and during lower rates of angiotensin infusion were plotted against concurrent plasma angiotensin II concentrations, a straight-line relationship was observed. This relationship also held for the higher rates of infusion in some subjects. 3. During infusion at a standard rate of 4 ng min−1 kg−1 the rise in plasma angiotensin II concentration varied widely from subject to subject. 4. There was a significant negative relationship between this increase and the threshold of the pressor response to angiotensin. 5. There was a significant positive relationship between the threshold of the pressor response and the basal concentrations of renin and angiotensin II. 6. These results suggest that angiotensin normally present in blood lies within or close to a range capable of affecting blood pressure.

Morphology and cyclooxygenase-2 and renin expression in the kidney of young spontaneously hypertensive rats

2021 ◽  
pp. 030098582110526
Author(s):  
Carmen G. Mondragón-Huerta ◽  
Rocío Bautista-Pérez ◽  
Luis A. Baiza-Gutman ◽  
María L. Escobar-Sánchez ◽  
Leonardo Del Valle-Mondragón ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Expression Patterns ◽  
Cyclooxygenase 2 ◽  
Renal Tubules ◽  
Hypertensive Rats ◽  
Plasma Urea ◽  
Spontaneously Hypertensive ◽  
Plasma Angiotensin

The kidneys play an important role in blood pressure regulation under normal and pathological conditions. We examined the histological changes and expression patterns of cyclooxygenase-2, renin, and (pro)renin receptor (PRR) in the renal cortex of prehypertensive spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKYs). Moreover, blood pressure and plasma urea, creatinine, angiotensin II, and angiotensin (1–7) levels were measured. The results showed that both strains had similar blood pressure and plasma urea and creatinine levels. The glomerular area, basement membrane thickness, collagen fiber content, and arterial wall thickness were greater in SHRs than in WKYs. By immunohistochemistry, cyclooxygenase-2 was localized in the macula densa and renal tubules of both strains. In SHRs, cyclooxygenase-2 was detected in a larger number of tubules, and the cortical expression of cyclooxygenase-2 was also increased. In both strains, PRR and renin were localized in the tubular epithelium and juxtaglomerular cells, respectively. In SHRs, PRR immunolocalization was increased in the glomerulus. The cortical expression of immature renin was markedly increased in SHRs compared to that in WKYs, while renin was significantly decreased. These changes were associated with higher plasma angiotensin II levels and lower plasma angiotensin (1–7) levels in SHRs. The results indicate that the kidneys of SHRs showed morphological changes and variations in cortical expression patterns of PRR, cyclooxygenase-2, and renin before the development of hypertension.

Central renin-angiotensin system and the pathogenesis of DOCA-salt hypertension in rats

1986 ◽  
Vol 251 (2) ◽  
pp. H261-H268 ◽  
Author(s):  
Y. Itaya ◽  
H. Suzuki ◽  
S. Matsukawa ◽  
K. Kondo ◽  
T. Saruta
Keyword(s):  
Blood Pressure ◽  
Fluid Intake ◽  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Vasopressin ◽  
Baroreceptor Reflexes ◽  
Salt Hypertension ◽  
The Brain

The antihypertensive effect of blockade of the brain renin-angiotensin system (brain RAS) was investigated in DOCA (deoxycorticosterone acetate)-salt hypertensive rats. Continuous intracerebroventricular (ICV) administration of SQ14225 (SQ; 1.25 micrograms X 0.5 microliter-1 X h-1) for 7 days attenuated the increase in blood pressure (99 +/- 5 vs. 116 +/- 4 mmHg on the 7th day) and also reduced the elevation of blood pressure (157 +/- 7 vs. 138 +/- 6 mmHg) in these hypertensive rats. Attenuation of increasing blood pressure in the developing phase following ICV SQ treatment was accompanied by decrease of fluid intake and prevention of elevation of the plasma vasopressin. In the established phase, in addition to reduction of the plasma vasopressin and decrease of fluid intake, restoration of the impaired baroreceptor reflexes was brought about by ICV SQ treatment. These results indicate that the brain RAS strongly influences the regulation of blood pressure in DOCA-salt hypertensive rats and that its mechanism of action is closely related to changes in sodium excretion, vasopressin, and the baroreceptor reflexes.

Afferent arteriolar diameter in DOCA-salt and two-kidney one-clip hypertensive rats

1983 ◽  
Vol 245 (6) ◽  
pp. F755-F762 ◽  
Author(s):  
B. M. Iversen ◽  
L. Morkrid ◽  
J. Ofstad
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Afferent Arteriole ◽  
Cortical Layers ◽  
Hypertensive Rats ◽  
Salt Hypertension ◽  
Nephron Loss ◽  
Microsphere Method ◽  
Arteriolar Diameter ◽  
Equal Thickness

The afferent arteriolar diameter (dAA) was investigated during development of hypertensive renal disease in normal and uninephrectomized control rats, in chronic DOCA-salt (DOCA), post-DOCA (p-DOCA), and chronic two-kidney one-clip (2K-1C) hypertensive rats, and in post-two-kidney one-clip (p-2K-1C) normotensive rats. dAA was measured by the microsphere method. Nephron loss was present in the kidneys exposed to elevate blood pressure. The dAA was reduced from 19.9 to 17.2 micron in the DOCA group (P less than 0.001) and from 19.1 to 16.3 micron in the nonclipped kidneys in the 2K-1C group (P less than 0.001). The dAA increased from 19.9 to 20.7 micron in the p-DOCA group. Afferent arteriolar dilatation from 19.1 to 21.0 micron (P less than 0.001) was present about 50 days after clipping in the 2K-1C group; in the clipped kidneys the dAA returned to normal (18.9 micron) after declipping. No relation between the dAA and plasma renin concentration was observed. In all models dAA was the same in three cortical layers of equal thickness. Accordingly, chronic renal DOCA-salt hypertension constricts the afferent arteriole with angiotensin-independent mechanisms. Autoregulatory dilatation of the afferent arteriole seems to be maintained for at least 50 days. When the hypertension is moderate, dAA in damaged kidneys may be dilated.

Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus

1996 ◽  
Vol 271 (1) ◽  
pp. R73-R83 ◽  
Author(s):  
D. A. Giussani ◽  
R. A. Riquelme ◽  
F. A. Moraga ◽  
H. H. McGarrigle ◽  
C. R. Gaete ◽  
...  
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
High Altitude ◽  
Chronic Exposure ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Pronounced Increase ◽  
Plasma Vasopressin ◽  
Plasma Angiotensin

We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.

Plasma Concentrations of Catecholamines in Two Strains of Spontaneously Hypertensive Rats at Different Ages

1981 ◽  
Vol 61 (s7) ◽  
pp. 199s-202s ◽  
Author(s):  
P. Ferrari ◽  
G. B. Picotti ◽  
E. Minotti ◽  
G. P. Bondiolotti ◽  
A. M. Caravaggi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Concentrations ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Adult Rats ◽  
Plasma Adrenaline ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Normotensive Strain ◽  
Noradrenaline And Adrenaline

1. Blood pressure was measured and plasma levels of noradrenaline and adrenaline were determined radioenzymatically under basal conditions and after 10% blood volume reduction in blood drawn through catheters previously implanted in young and adult rats of two different genetically hypertensive strains: the Kyoto strain (SHR) and the Milan strain (MHS), and in their respective controls: Wistar—Kyoto strain (WKY) and Milan normotensive strain (MNS). 2. Under basal conditions no differences were observed between plasma noradrenaline and adrenaline levels in SHR and MHS rats and in the controls, at any age. Haemorrhage produced a greater fall in the blood pressure (P &lt; 0.01) of young and adult hypertensive strains (SHR-MHS) than in WKY and MNS rats, and a greater rise in plasma adrenaline (P &lt; 0.01). 3. These results suggest that: (a) there may be differences in involvement of the sympathetic nervous system in the pathogenesis of hypertension in SHR and MHS rats but not such as to cause differences in plasma catecholamine levels in either young or adult rats; (b) haemorrhage activates the sympatho—adrenal systems more in SHR and MHS rats, than in controls, and the greater percentage fall in blood pressure is probably due to a difference in reflex venoconstriction.

scholarly journals R-PEP-27, a Potent Renin Inhibitor, Decreases Plasma Angiotensin II and Blood Pressure in Normal Volunteers

1994 ◽  
Vol 7 (4 Pt 1) ◽  
pp. 295-301 ◽  
Author(s):  
R. M. Zusman ◽  
K. Y. Hui ◽  
J. Nussberger ◽  
D. M. Christensen ◽  
J. Higgins ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Inhibitor ◽  
Normal Volunteers ◽  
Plasma Angiotensin
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