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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible role of increased vascular reactivity in the mechanism of experimental hypertension was studied by measurements of the critical opening pressure (COP) of tail vessels in conscious rats. In hypertension induced by administration of desoxycorticosterone acetate (DOCA) and replacement of the drinking water by 1% NaCl solution (DOCA-NaCl hypertension), and in one-kidney Goldblatt renovascular hypertension, the raised level of blood pressure was associated with an increased COP of the tail vessels when measured both before and after ganglionic blockade. In rats treated with either DOCA alone or 1% NaCl alone there was no significant increase in systolic blood pressure (SBP) or COP relative to the corresponding controls. In all four experimental series intravenous infusion of angiotensin or norepinephrine in conscious ganglion-blocked rats produced dose-dependent increases in SBP and COP. In DOCA-NaCl hypertensive rats but not in renovascular hypertensives, nor in rats treated with DOCA alone or 1% NaCl alone, the increase in COP for a given increment in dose of angiotensin or norepinephrine was significantly greater than in the control rats. It is concluded that in DOCA-NaCl hypertension there is a true increase in the reactivity of the smooth muscle of the resistance vessels to angiotensin and norepinephrine. In renovascular hypertension this is not the case and other factors must therefore be involved in causing the increased blood pressure and COP.
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PMID:Critical opening pressure and reactivity of tail vessels in conscious hypertensive rats. 0 1

1. Noradrenaline content of several rat brain stem and hypothalamic nuclei falls transiently at 72 h after initiation of renovascular hypertension (one-kidney Goldblatt model). 2. Tyrosine hydroxylase activity is significantly reduced in posterior, paraventricular and periventricular nuclei of hypothalamus at this time but returns to control value by 7 days. 3. Treatment with hydrallazine, 5 mg/kg intraperitoneally, twice daily or methaoxamine, 5 mg/kg, three times daily for 3 days respectively raises and lowers the noradrenaline content of brain nuclei, suggesting that short-term changes in noradrenaline may be secondary to afferent baroreceptor input. 4. At later times after the development of renovascular hypertension (7 and 28 days) activity of phenylethanolamine-N-methyl transferase is increased in the nucleus of the solitary tract and the locus coeruleus. 5. Brain catecholamines may participate both early in the development and later in the maintenance of renovascular hypertension.
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PMID:Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. 3 99

1. Hypertension was induced in rats by renal artery clip with the contralateral kidney removed (Goldblatt I) or left intact (Goldblatt II). 2. Plasma noradrenaline was increased 62% in the Goldblatt I animals after 3 weeks. 3. Hypothalamic tyrosine hydroxylase and dopamine beta-hydroxylase activities, and the concentration of noradrenaline were increased in the Goldblatt I animals after 3 weeks. 4. Enhanced hypothalamic noradrenaline synthesis may be a pathogenic factor in Goldblatt I renovascular hypertension.
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PMID:Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. 3

Rats with experimental renovascular hypertension were treated with high doses of beta-blocking agents. Pindolol 10 mg/kg per day increased Goldblatt-type hypertension, whereas Propranolol 100 mg/kg per day showed an antihypertensive effect. A linear correlation between the weight of the left-heart ventricle and the systolic blood pressure was found in animals treated with Pindolol as well as in untreated Goldblatt rats. On the contrary, the weights of the left-heart ventricle were significantly higher in those animals treated with Propranolol than in the other groups. The results show that Pindolol in high doses, possibly on account of its sympathomimetic activity, leads to an increase in Goldblatt hypertension, but does not influence the pressure-dependent progression of left-heart hypertrophy. On the other hand, Propranolol, possibly on account of a cardiodepressory effect, leads to a decrease in blood pressure.
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PMID:[High dose betablocker treatment in experimental renal hypertension (author's transl)]. 4 62

Beta blockade was instituted in 10 patients with renovascular hypertension due to renal artery stenosis or thrombosis. The treatment was very effective in unilateral stenosis with a normal contralateral kidney (2 kidney Goldblatt) and in fibromuscular dystrophy of the renal artery. On the other hand many failures were observed in hypertension with a single kidney (1 kidney Goldblatt) and in renovascular hypertension with complex lesions or associated renal failure. Although a clear relationship was often observed between the increased plasma renin activity and the antihypertensive effect of beta blockade, this association was sometimes completely erroneous. Beta blockade, which is easy to perform, should be tried out systematically in renovascular hypertension, but, when no result is observed, this therapeutic test should not exclude surgical management thereafter.
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PMID:[Renovascular hypertension and beta blockers. Theoretical and practical implications]. 4 14

The degree of round cell infiltration around hypertensively damaged heart arteries in one kidney Goldblatt hypertensive mice is more pronounced in haired mice with normal thymus function than in their nude littermates with genetic aplasia of the thymus. The level of hypertension and the prognoses for the hypertensive mice are, however, not influenced by the presence of thymus and thymus derived T cells. The results give evidence that delayed type immune reactions are involved in the hypertensive vascular disease in mice, but fail to support the assumption that they have pathogenic importance for either the level of hypertension or the prognoses of the one kidney Goldblatt hypertensive mice.
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PMID:Studies elucidating the importance of thymus on the degree of increased blood pressure and vascular disease in renal hypertensive mice. A comparison of the disease in nude and haired littermates. 12 33

Hypertensive Goldblatt-rats have higher than normal Na-appetite and an enhanced Na-output. They have normal plasma Na- and K-concentration and kidney weight but a significantly reduced plasma volume. The amount of renal membrane protein and the renal Na-K-ATPase-activity of hypertensive rats was found to be significantly below that of controls. In order to evaluate the role of Na-appetite, Na-excretion rate and renal Na-K-ATPase-activity in the electrolyte balance, Goldblatt-rats with a stable hypertension and control animals were put for 8 days on a Na-free diet. Na-excretion rate of control rats reached a minimum (13 muEq/100 g x 24 hr) within 5 days and was maintained on this level up to the end of the experiment. Na-free diet did not alter either the kidney weight or the amount of membrane protein of the animals. However, in salt-free fed control rats total renal Na-K-ATPase-activity was found elevated by about 10% as compared to animals maintained on normal diet. Goldblatt-rats continuously excreted significantly higher amounts of Na (35 muEq/100 g x 24 hr), had sharply reduced plasma volume and plasma Na- concentration. The renal Na-K-ATPase-activity should no adaptation in gold blatt-rats. In all animals studied the rate of Na-excretion showed a close indirect correlation with the renal Na-K-ATPase-activity. It is concluded, that Goldblatt-rats depend on dietary Na to a higher extent than controls because of their reduced capacity to retain Na. The increased Na-appetite of hypertensive rats is a factor secondary to Na-loss.
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PMID:Interdependence of Na-excretion, plasma electrolytes, plasma volume and renal Na-K-ATPase-activity in hypertensive rats. 13 99

Preexisting increase of plasma renin activity in hypertension seems to indicate an effective hypotensive action of adrenergic beta-receptor antagonists. In spite of marked elevation of plasma renin activity in Goldblatt-rats, the beta-blocker Pindolol failed to lower the blood pressure. On the contrary, high doses of this substance led to an acceleration of the Goldblatt-type hypertension, perhaps because of the intrinsic sympathomimetic activity of Pindolol. These findings support the conception that beta-blockers are effective in lowering the blood pressure only in hypertension with stimulated renin secretion, which is caused by an increased activity of the sympathetic nervous system. Plasma renin activity was not altered by Pindolol. There existed a linear relationship between blood pressure and left-ventricular weight in all groups of rats, which was not impaired by Pindolol in all used doses.
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PMID:[The influence of the beta-blocking agent pindolol on blood pressure and heart weight of rats with Goldblatt-type hypertension (author's transl)]. 14 Feb 70

1. Clonidine (6 mg of base/l of water) was given as drinking fluid to normotensive rats or rats with established or early hypertension. 2. Spontaneous hypertensive rats (6 months old: average dose of clonidine, 0.6 mg 24 h-1 kg-1) showed a sustained fall in blood pressure over 3 weeks. 3. The same clonidine solution given for 6 weeks to two-kidney Goldblatt rats with early-stage hypertension (average dose of clonidine: 1 mg 24 h-1 kg-1) or spontaneously hypertensive rats (clonidine dose: 1 mg) induced a fall in mean blood pressure, but no change in normotensive rats. 4. Replacement of clonidine by water induced hypertension and lability which led to death in hypertensive but not in normotensive rats.
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PMID:Effect of chronic clonidine treatment and its abrupt cessation on mean blood pressure of rats with a normal or an elevated blood pressure. 15 30

SQ 14,225 (D-3-mercapto-2-methylpropanoyl-L-proline) markedly lowered the blood pressure of the renin-dependent aortic-ligated and two-kidney Goldblatt hypertensive rat and failed to reduce blood pressure in the one-kidney Goldblatt hypertensive rat. In the two-kidney Goldblatt rat, SQ 14,225 (p.o.) was about 10 times as potent as teprotide, the nonapeptide SQ 20,881 (s.c.). Oral doses of SQ 14,225 moderately reduced the blood pressure of the Wistar-Kyoto spontaneously hypertensive rat but not that of the normotensive Wistar-Kyoto rat. Bilateral nephrectomy abolished the antihypertensive activity of SQ 14,225 in the spontaneously hypertensive rat. SQ 14,225 and SQ 20,881 elicited parallel dose-response curves in the two-kidney renal hypertensive rat. Post-treatment of spontaneously hypertensive rats with either agent failed to augment the antihypertensive effect produced by effective doses of the other agent. The results suggest that SQ 14,225 acts primarily by inhibiting the renin-angiotensin system to reduce elevated blood pressure, especially in presumably renin-dependent models of hypertension.
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PMID:Antihypertensive activity in rats for SQ 14,225, an orally active inhibitor of angiotensin I-converting enzyme. 20 93


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