Blood Pressure Response to Central and Peripheral Injection of Angiotensin II and 8-C-Phenylglycine Analogue of Angiotensin II in Rats with Experimental Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 403s-406s
Author(s):  
B. A. Schoelkens ◽  
W. Jung ◽  
R. Steinbach
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Spontaneous Hypertension ◽  
Experimental Hypertension ◽  
Central Administration ◽  
Spontaneously Hypertensive ◽  
Old Rats

1. We have compared the effect of central and peripheral administration of angiotensin II and (1-succinamoyl-5-valine-8-phenylglycine)angiotensin II on blood pressure of male conscious unrestrained rats with normal blood pressure, and with spontaneous hypertension or chronic renal hypertension. 2. After central and peripheral injection of angiotensin II all rats exhibited a significant dose-related increase in blood pressure. 3. Administration of the analogue was without effect in normotensive rats. Ten-weeks-old rats with spontaneous hypertension showed a significant blood pressure decrease after central injection, but an increase after peripheral injection. This centrally induced decrease could not be observed in spontaneously hypertensive rats 14 weeks old. In these animals the analogue increased the blood pressure. In rats with chronic renal hypertension in contrast to peripheral injection, central administration decreased the pressure significantly. 4. Plasma renin activity was not changed after central injection of the analogue in normotensive rats. 5. These observations suggest the participation of the intrinsic brain isorenin-angiotensin system in central blood pressure regulation in these forms of experimental hypertension.

scholarly journals Effect of chronic nifedipine treatment on blood pressure and adrenergic responses of isolated mesenteric artery in young rats with developing spontaneous hypertension

2009 ◽  
pp. 921-925
Author(s):  
A Zemančíková ◽  
J Török
Keyword(s):  
Blood Pressure ◽  
Mesenteric Artery ◽  
Calcium Influx ◽  
Age Groups ◽  
Spontaneous Hypertension ◽  
Experimental Hypertension ◽  
Rapid Phase ◽  
Spontaneously Hypertensive ◽  
Old Rats ◽  
Hypertension Development

It is documented that in chronic hypertensive state there is an increased vasodepressor response to calcium channel antagonists such as the dihydropyridine derivate nifedipine. This effect is generally proportional to initial blood pressure as was demonstrated in several models of experimental hypertension. In the present study we investigated the effect of chronic nifedipine treatment on the development of cardiovascular system in young spontaneously hypertensive rats (SHR) in order to evaluate whether it could prevent the abnormalities leading to hypertensive state. Four- and eight-week-old rats were treated with nifedipine (50 mg/kg/day) for 4 weeks. Blood pressure of nifedipine-treated SHR remained at the initial level in contrast to their untreated controls where it continued to increase. In both age groups, chronic nifedipine administration reduced neurogenic contractions of isolated superior mesenteric artery, but did not significantly affect the dose-response curve to exogenous noradrenaline in 8-week-old rats. In contrast, maximum response to noradrenaline was significantly attenuated in mesenteric artery of 12-week-old nifedipine-treated SHR. We can presume that the antihypertensive effect of nifedipine is similar in both stages of spontaneous hypertension development, but the mechanisms involved might be different. It seems that chronic reduction of calcium influx during the rapid phase of pathological blood pressure increase in SHR may eliminate the effect of enhanced sympathetic tone, which may have unfavorable consequences on cardiovascular structure and function.

Blood pressure responsiveness during the development of hypertension in the conscious spontaneously hypertensive rat

1985 ◽  
Vol 63 (10) ◽  
pp. 1258-1262 ◽  
Author(s):  
Corey B. Toal ◽  
Frans H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rat ◽  
Blood Pressure Response ◽  
Receptor Occupancy ◽  
Pressure Response ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Freely Moving ◽  
Wistar Kyoto

Blood pressure responsiveness to iv noradrenaline and angiotensin II was studied in conscious, freely moving, age-matched spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats from 4 to 16 weeks of age. At 4 and 6 weeks the SHR showed small, but nonsignificant increases in responsiveness compared with WKY to both noradrenaline and angiotensin II. At 8 weeks they exhibited similar responses to the WKY. Subsequently, at 12 and 16 weeks decreased responsiveness to noradrenaline (nonsignificant) and angiotensin II (p < 0.05 at 12 and 16 weeks) was observed in SHR versus WKY. At 16 weeks of age, hexamethonium caused potentiation of the blood pressure response to noradrenaline and angiotensin II, but to the same degree in the two strains. Captopril at this age did not elicit potentiation to noradrenaline or angiotensin II in either strain. These results indicate that there is no rise in blood pressure responsiveness to circulating pressor agents, parallel to the development of hypertension in SHR. Increased receptor occupancy or more active attenuating reflexes in SHR versus WKY appear not to be involved in the absence of hyperresponsiveness in intact consious SHR at 16 weeks of age.

Central angiotensin II-induced responses in spontaneously hypertensive rats

1977 ◽  
Vol 232 (4) ◽  
pp. H426-H433 ◽  
Author(s):  
W. E. Hoffman ◽  
M. I. Phillips ◽  
P. G. Schmid
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressure Effects ◽  
Spontaneous Hypertension ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Vascular Responsiveness ◽  
Vascular Sensitivity ◽  
Wistar Kyoto ◽  
The Brain

The brain isorenin angiotensin system has been implicated in the development of spontaneous hypertension by several investigators. The experiments reported here were designed to test the responsiveness of unanesthetized spontaneous hypertensive (SH) rats to intracerebroventricular angiotensin II injections compared to Wistar-Kyoto (WK) normotensive controls. The results indicate that there is no difference between SH and WK animals in drinking responses or antidiuretic hormone release to central angiotensin II injections; however, an increased pressor responsiveness to intraventricular angiotensin II in SH as compared to WK was observed. The results of intravenous infusions of pressor substances in these experiments and reports by other investigators suggest that the increased blood pressure effects to central angiotensin are due to three possible factors: 1) increased vascular responsiveness of SH to vasoconstrictor substances in general, 2) increased vascular sensitivity of SH rats to sympathetic outflow, and 3) decreased baroreceptor reflexes to acute increases in blood pressure. We suggest that the brain isorenin-angiotensin system may be involved in spontaneous hypertension by increased production of angiotensin II or by activation of a potentiated sympathetic system, but not by a generalized increased sensitivity of brain receptors to central angiotensin.

Effect of Propranolol on Blood Pressure in Normal and Hypertensive Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 101s-103s
Author(s):  
J. Conway ◽  
K. Darwin ◽  
A. Hilditch ◽  
B. Loveday ◽  
M. Reeves
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Chronic Treatment ◽  
Spontaneous Hypertension ◽  
Beta Blockade ◽  
Experimental Hypertension ◽  
Hypertension Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Propranolol Treatment

1. Propranolol has been given orally in a dose sufficient to achieve beta-blockade throughout the day in normal rats, renal hypertensive animals with and without contralateral nephrectomy, spontaneously hypertensive and deoxycorticosterone (DOCA) hypertensive rats. The drug was given either after hypertension had become fully established or during the phase of rising blood pressure. 2. With this treatment, heart rate was reduced by approximately 100 beats/min in all experimental groups. 3. In established hypertension, treatment with propranolol for 7–9 days was ineffective in lowering blood pressure in any of the models of experimental hypertension. It also had no effect on blood pressure in normal animals. 4. Chronic treatment with propranolol during the phase of rising blood pressure had no effect in renal hypertensive animals. In spontaneous hypertension, the rise in blood pressure was limited to 28 mmHg with propranolol treatment as compared with 58 mmHg in control animals. Likewise, in DOCA hypertension, the rise in pressure was limited to 18 mmHg as compared with 46 mmHg in control animals.

Comparative Pharmacology of New Specific Angiotensin Antagonists

1974 ◽  
Vol 48 (s2) ◽  
pp. 19s-21s
Author(s):  
B. A. Schoelkens
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Renal Hypertension ◽  
Antagonistic Activity ◽  
Conscious Rats ◽  
Blood Pressures ◽  
Colon Ascendens

1. The angiotensin II antagonism by newly synthesized 8-C-phenylglycine analogues of [5-isoleucine]angiotensin II in different preparations was investigated in vitro and in vivo. 2. All analogues competitively inhibited the myotropic effect of angiotensin II on the isolated colon ascendens of the guinea-pig and the stomach of the rat. 3. In normotensive dogs, cats, rabbits, guinea-pigs and rats the blood pressure response to infused angiotensin II was inhibited by the antagonists. The angiotensin II-induced fall in renal blood flow in the dog was blocked during infusion of the analogues. Acute renal hypertension in rats was significantly decreased. Of conscious rats variously with normal blood pressures, spontaneous hypertension and chronic renal hypertension, only in the last group could a marked uniform fall in blood pressure be demonstrated. The central pressor effect of angiotensin II was also inhibited in conscious rats. 4. 8-C-Phenylglycine analogues of [5-isoleucine]-angiotensin II exhibit a specific antagonistic activity to endogenous and exogenous angiotensin II.

Exaggerated blood pressure response to angiotensin II in patients with Cushing's syndrome due to adrenocortical adenoma

1994 ◽  
Vol 131 (6) ◽  
pp. 582-588 ◽  
Author(s):  
Gen Yasuda ◽  
Hiroshi Shionoiri ◽  
Satoshi Umemura ◽  
Izumi Takasaki ◽  
Masao Ishii
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cushing’S Syndrome ◽  
Blood Pressure Response ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Cushing's Syndrome ◽  
Adrenocortical Adenoma ◽  
Angiotensin System ◽  
Renin Angiotensin

Yasuda G, Shionoiri H, Umemura S, Takasaki I, Ishii M. Exaggerated blood pressure response to angiotensin II in patients with Cushing's syndrome due to adrenocortical adenoma. Eur J Endocrinol 1994:131:582–8 ISSN 0804–4643 We studied the roles played by the renin-angiotensin system in inducing hypertension in nine patients with Cushing's syndrome (CS) resulting from adrenocortical adenoma, and compared them with those in patients with primary aldosteronism (PA), renovascular hypertension (RVH) and essential hypertension (EH). In the CS group, each parameter, including serum potassium, plasma renin activity, plasma aldosterone, deoxycorticosterone and corticosterone concentrations, is within the normal range. However, plasma renin activity in the CS group was lower than that in the RVH group but higher than that in the PA group, and plasma aldosterone concentration was lower than that in each RVH or PA group. These findings indicated that the CS group had a different type of hypertension from that in either RVH or PA, in which the renin angiotensin system or mineralocorticoids play an important role in hypertension. Meanwhile, captopril (50 mg) administration either with or without indomethacin pretreatment decreased the mean blood pressure in the CS group, although captopril failed to change it in the PA group or in normal subjects. Furthermore, the pressor response to exogenous angiotensin II in the CS group was higher than that in the RVH or EH group, but was not different from that in the PA group. Thus, the hypertension in patients with CS due to adrenocortical adenoma appears to be mediated through a change in the renin-angiotensin system in the form of exaggerated pressor responses to angiotensin II. G Yasuda, Second Department of Internal Medicine, Yokohama City University School of Medicine, 3-46 Urafune, Minami, Yokohama 232, Japan

Inhibition of Adrenaline-Forming Enzyme in the Brain Prevents One-Kidney, One-Clip Hypertension and Deoxycorticosterone Acetate-Salt Hypertension in the Rabbit

1982 ◽  
Vol 63 (6) ◽  
pp. 573-576 ◽  
Author(s):  
C. Rosendorff ◽  
J. R. Melamed ◽  
M. L. Hurwitz ◽  
A. Coull ◽  
A. Jarvis
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Renal Hypertension ◽  
Pressure Rise ◽  
Deoxycorticosterone Acetate ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Salt Hypertension ◽  
The Mean ◽  
The Brain

1. Phenylethanolamine N-methyltransferase (PNMT) converts noradrenaline into adrenaline and brain PNMT is elevated in spontaneously hypertensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In view of the evidence for the involvement of central adrenergic neurons in renal hypertension, we measured the blood pressure response in one-clip, one-kidney Goldblatt hypertensive and DOCA-salt hypertensive rabbits to the PNMT inhibitor SK&F 64139, injected into the lateral cerebral ventricles. 2. Intracerebroventricular injection of SK&F 64139 (10 μg/kg) significantly attenuated the mean arterial blood pressure rise in one-clip, one-kidney and DOCA-salt rabbits, at 4 and 8 weeks. 3. These findings support the idea that hypertension in this animal model requires an intact adrenaline biosynthetic process, and that central catecholaminergic neurons may be involved in the pathogenesis of low-renin volume dependent forms of hypertension.

Arterial Wall Renin and Renal Venous Renin in the Hypertensive Rat

1979 ◽  
Vol 56 (1) ◽  
pp. 41-46 ◽  
Author(s):  
Josephine B. Garst ◽  
S. Koletsky ◽  
P. E. Wisenbaugh ◽  
Magdalena Hadady ◽  
D. Matthews
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Arterial Wall ◽  
Renal Hypertension ◽  
Spontaneous Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Long Duration

1. Infusion of sufficient renin to raise the blood pressure of normal rats to hypertensive levels resulted in increased renin in the arterial wall. 2. Arterial wall renin and renal venous renin were normal in younger spontaneously hypertensive rats, but in older spontaneously hypertensive rats arterial wall renin was significantly increased and renal venous renin was significantly decreased. 3. Arterial wall renin in rats with either acute or chronic two-kidney Goldblatt renal hypertension was significantly increased, whereas circulatory renin was elevated in the former, but depressed in the latter. 4. Arterial wall renin may play a role in the maintenance of acute and chronic renal hypertension and also perhaps of spontaneous hypertension of long duration in older rats.

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