Accelerated Hypertension in the Rat: Relation between Renin, Renal Vascular Lesions, Salt Intake and Blood Pressure

1976 ◽  
Vol 51 (s3) ◽  
pp. 69s-71s ◽  
Author(s):  
Sauwaluck Chusilp ◽  
A. S. P. Hua ◽  
Priscilla Kincaid-Smith
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Tap Water ◽  
Plasma Renin ◽  
Renin Activity ◽  
Vascular Lesions ◽  
Control Group ◽  
Group 3 ◽  
Renal Vascular ◽  
Control Group Group

1. Complete ligation of the aorta between the origins of the two renal arteries in the rat produces a predictable form of accelerated hypertension. Changes in the blood pressure, plasma renin activity and renal histological lesions have been studied. 2. Group 1 rats and their control group (group 2) received tap water, and group 3 and its control group (group 4) received sodium chloride solution (0·154 mol/l) in place of tap water, for 4 weeks before aortic ligation. In the experimental groups 1 and 3, complete ligation was carried out. In groups 2 and 4 the aorta and renal arteries were exposed, but not ligated. Interlobular artery lesions were studied on a blind basis and graded 0–4 according to severity. 3. Groups 1 and 3 developed severe hypertension. In group 1 the raised mean arterial pressure showed a significant correlation with increased plasma renin activity. Both mean arterial pressure and plasma renin activity also showed a significant correlation with changes in interlobular arteries. In group 3 the raised mean arterial blood pressure did not show a significant correlation with the depressed plasma renin activity, or with changes in interlobular arteries. A significant correlation was, however, found between plasma renin activity and interlobular artery lesions in group 3. 4. These results suggest that the renin-angiotensin system may influence renal vascular lesions through some mechanism independent of the blood pressure.

scholarly journals Chronic effects of Bunitrolol and Pindolol on blood pressure,heart rate,vascular lesions,and plasma renin activity in hypertensive rats.

1982 ◽  
Vol 32 (4) ◽  
pp. 742-745 ◽  
Author(s):  
Yukio HASEGAWA ◽  
Takushi X. WATANABE ◽  
Koichiro KAWASHIMA ◽  
Hirofumi SOKABE ◽  
Ken SAITO
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Vascular Lesions ◽  
Hypertensive Rats ◽  
Chronic Effects

Natriuretic Response to Head-Out Immersion in Humans with Recent Kidney Transplants

1993 ◽  
Vol 85 (4) ◽  
pp. 471-477 ◽  
Author(s):  
Ton J. Rabelink ◽  
Karin A. van Tilborg ◽  
Ronald J. Hené ◽  
Hein A. Koomans
Keyword(s):  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Renin Activity ◽  
Control Group ◽  
Control Subjects ◽  
Renal Vascular

1. Recently implanted kidneys may have decreased flexibility to adjust sodium excretion to volume challenges, since modulation by renal sympathetic nerve activity is absent. To examine this hypothesis, we studied the natriuretic response to head-out water immersion in eight patients with well-functioning renal allografts of 37 days (range 24–56 days), at a time when renal re-innervation has probably not occurred. 2. By the third hour of head-out water immersion, sodium excretion had increased equally in the patients (from 120 +21 to 204 +37 μmol/min) and in eight healthy control subjects (from 105 +9 to 191+19 μmol/min). 3. Glomerular filtration rate was 60 + 6 ml/min in the patients and 113 +6 ml/min in the control subjects, and did not change upon head-out water immersion. Estimated renal plasma flow increased upon head-out water immersion in the control group but not in the patients. Blood pressure decreased similarly in both groups. The renal vascular resistance, calculated from these data, decreased in response to head-out water immersion in the control subjects but not in the renal transplant patients. 4. Head-out water immersion suppressed plasma renin activity only in the normal group, whereas the plasma aldosterone level was suppressed in both groups. The natriuretic response in patients was associated with about 3-fold elevated plasma levels of atrial natriuretic peptide. 5. Since renal re-innervation at 37 days after transplantation is very unlikely, these data suggest that inact renal innervation is not mandatory for a normal natriuretic response to head-out water immersion in humans. However, sympathetic modulation might be involved in the decrease in renal vascular resistance and plasma renin activity normally observed during immersion.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

Sign in / Sign up

Export Citation Format

Share Document