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

Cyclic analogs of bradykinin (CBK) and kallidin (CK) have a weak myotropic activity and a marked and prolonged hypotensive effect unlike linear bradykinin (BK) and kallidin (K) which produce a short-term hypotension and considerable contraction of rat uterus smooth muscles. Myotropic effects of BK and CK were significantly inhibited by phentolamine, methysergide, papaverine and verapamil. Atropine, diphenhydramine and propranolol have no influence on the kinin-induced myotropic responses. The prolonged decrease in blood pressure induced by CBK and CK is observed in un- and anesthetized normotensive, spontaneously hypertensive rats and rats with renovascular hypertension and is absent from anesthetized cats and guinea-pigs. This indicates the species specificity of cyclokinins. Indomethacin, diphenhydramine and methysergide failed to influence the BK- and CK-induced hypotensive effects on anesthetized rats. CaCl2 did not influence the magnitude of the hypotensive effect of BK and CK, however, it significantly shortened the duration of the CK-induced hypotensive effect. In vitro CBK and CK inhibited activity of kininase II in a similar manner (at a concentration range of 10(-5) M) but to a less extent than BK (10(-7)-10(-6) M). It is suggested that the hypotensive effect of CK is mediated at least partly via Ca2+-dependent systems and inhibition of kininase II.
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PMID:[Mechanism of action of cyclokinins]. 631 9

Renal hypertension (one-clip, two kidney) developed to a lower level in essential fatty acid (EFA)-deficient rats than in controls on a complete diet. Body weight gain was the same in both clipped groups. Hypertension in rats on an EFA-deficient diet supplemented with linoleic acid (corn oil) was comparable to that in rats on a complete diet. Plasma renin activity was significantly higher in both hypertensive groups. However, in the EFA-deficient groups the difference between hypertensive and sham-operated rats was 63% less than in the "control" groups. Indomethacin potentiated the development of renal hypertension of the control group. Addition of 3.5% linoleic acid (corn oil) to a complete diet blunted the development of hypertension. It is suggested that in the EFA-deficient rats, a lack of endogenous prostaglandin biosynthesis is not responsible for the attenuated development of renal hypertension.
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PMID:Attenuated development of renal hypertension in essential fatty acid-deficient rats. 636 59

Three weeks of treatment with arachidonic acid (250 mg/kg/day, s.c.) produced an antihypertensive effect in 16 week-old spontaneously hypertensive rats (SHR) as compared with vehicle treated rats. Indomethacin (4 mg/kg, s.c. B.I.D.), given concurrently with arachidonate, abolished the antihypertensive effect. Plasma catecholamines were not altered by the arachidonate treatment, but blood pressure increments after spinal cord stimulation or after intravenous administration of norepinephrine and angiotensin II in the pithed rat were diminished. Increments in plasma catecholamines in response to spinal cord stimulation were similar in both groups of pithed rats. These data demonstrate the antihypertensive effect of arachidonic acid in SHR with established hypertension. This beneficial effect seems to be mediated through cyclooxygenase metabolites, and might be related to reduced responsiveness of peripheral blood vessels to pressor stimuli.
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PMID:Effects of chronic arachidonate on blood pressure of spontaneously hypertensive rats. 641 21

Treatment of a 55-year-old woman with Raynaud's phenomenon and orthostatic hypotension secondary to lumbar sympathectomy performed for Raynaud's phenomenon is described. Indomethacin increased the blood pressure but caused severe gastrointestinal bleeding. It was possible to treat the symptoms of Raynaud's phenomenon with drugs generally used to treat hypertension without causing an undue decrease in blood pressure and, at the same time, to combat orthostatic hypotension with drugs to increase blood pressure.
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PMID:Simultaneous treatment of Raynaud's phenomenon and orthostatic hypotension. 661 39

Experiments on anesthesized normotensive rats (NR), spontaneous-hypertensive rats (SHR) and rats with experimental renovascular hypertension (RVR) were made to study the effect of prostaglandins (PG) - PGI2, PGE1, PGF2, and indomethacin on systemic hemodynamics, pressor reaction and cardiac component of the baroreflex. PGI1 (0.015 microgram/kg) PGE1 (5 micrograms/kg) produced marked hypotension which was more remarkable in RVR and SHR than in NR. The hypotensive effect of both PG was determined by peripheral vasodilatation. After administration of PGI2 and PGE1 the baroreflex appreciably rises in hypertensive rats. PGE2 (10 micrograms/kg) elevates arterial blood pressure in NR to a greater degree than in RVR and SHR. Indomethacin (10 mg/kg) raises the pressure by 33% in NR, by 16% in SHR and by 5% in RVR. At the same time baroreflex sensitivity in NR declines by 208%.
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PMID:[Hemodynamic reaction of normotensive and hypertensive rats to the administration of prostaglandins and indomethacin]. 675 30

The behaviour of active (AR) and inactive (IR) renin was studied in 48 hypertensive patients (37 with uncomplicated essential hypertension and 11 with reno-vascular hypertension) treated with indomethacin alone or with AR stimulating (bumetanide, tienilic acid, captopril) and inhibiting (atenolol) drugs before and after indomethacin addition. In 10 pts indomethacin (50mg q.i.d./3 days) reduced (p less than 0.05) AR and to a lesser extent IR. In 6 pts bumetanide (1 mg) increased (p less than 0.05) only AR and this effect was abolished by indomethacin. In 6 pts tienilic acid (250 mg) increased (p less than 0.05) only AR and this action was unchanged by indomethacin. In 11 renovascular pts captopril (100mg) increased AR (p less than 0.01) and lesser IR and both these effects were uninfluenced by indomethacin. In 11 essential hypertensive pts captopril (25mg b.i.d./3 days) increased only AR (p less than 0.02), but after 1 year both AR and IR were increased (p less than 0.05) and these effects were abolished by indomethacin. In all the above reported protocols we did never find any inverse correlation between either AR and IR values or their induced changes. These data suggest that prostaglandins stimulate, even if not to a similar extent, both AR and IR and that drugs, which stimulate renin either through or independently of PGs, did not cause any apparent interconversion of plasma IR into AR. In 6 pts atenolol (100 mg daily/6 days) reduced AR (p less than 0.05) and tended to increase IR. Indomethacin addition further decreased AR and reduced IR (both p less than 0.05 vs atenolol alone): however the proportion (% of total) of IR was still reduced. These findings suggest that beta 1-adrenoreceptors blockade exerts a divergent effect on active and inactive renin and that this action is not influenced by PGs synthesis inhibition.
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PMID:Effects of prostaglandins inhibition on changes in active and inactive renin induced by antihypertensive drugs. 675 7

Severe bradycardia and hypotension associated with the administration of organic nitrates or nitrites has been observed in patients with ischaemic heart disease and hypertension. Experiments were performed on rats to elucidate the mechanism by which these vasodilators may effect their anomalous bradycardia-hypotensive effect. In sodium pentobarbital (50 mg.kg-1, ip) anaesthetised rats of the Wistar strain, hypotension and a paradoxical bradycardia were observed following the intra-arterial injection of 10 microgram.kg-1 sodium nitroprusside or 1 mg.kg-1 arachidonic acid. Bilateral vagotomy abolished the bradycardia to both sodium nitroprusside and arachidonic acid but did not eliminate their hypotensive effects. Indomethacin (5 mg.kg-1) abolished the blood pressure and heart rate responses to arachidonic acid. However, indomethacin abolished only the bradycardia to sodium nitroprusside without reducing its effect on blood pressure. These data suggest that in the rat sodium nitroprusside can stimulate prostaglandin biosynthesis which then initiates a reflex bradycardia.
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PMID:Paradoxical bradycardia following the administration of sodium nitroprusside in the rat is abolished by indomethacin. 680 92

Renal prostaglandins play a role in the control of renin release during chronic sodium depletion, during the acute phase of renovascular hypertension and in experimental low output heart failure in conscious dogs. However, with marked inhibition of the renin-angiotensin system, the adrenergic nervous system and the renal prostaglandins, PRA was still 17 times normal during chronic sodium depletion. After blockade of the adrenergic nervous system and the renal prostaglandins, PRA was 10 times normal during the acute phase of one-kidney renovascular hypertension. These findings demonstrate that other important mechanisms, possibly both the renal vascular receptor (so-called baroreceptor) and the macula densa, were involved. Both PGI2 and PGD2 given intrarenally increased renin release in both filtering and nonfiltering kidneys, but PGI2 was more potent than PGD2. Available evidence favors a role of PGI2 and it seems likely that the site of action is on the JG cells. Indomethacin produced a profound drop in CCr and CPAH during sodium depletion and in experimental heart failure which demonstrates an important role for the renal prostaglandins in the control of renal arteriolar tone. An important incidental finding is that renal denervation combined with propranolol administration decreased PRA from very high levels to normal in 50% of the dogs with experimental low output heart failure and a concurrent striking natriuresis occurred.
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PMID:Renal prostaglandins, renin release, and renal hemodynamic function in high renin states. 700 Apr 61

This study examines the role that prostaglandins play in both the developmental and chronic phases of renovascular hypertension. Two 5-mg/kg doses of indomethacin were given to conscious dogs with renal denervation and receiving propranolol during the acute and chronic phases of one-kidney (1-KHT) and the acute phase of two-kidney (2-KHT) renovascular hypertension. Indomethacin produced striking reductions in plasma renin activity from the high level observed during the acute phase of both 1-KHT and 2-KHT. However, plasma renin activity failed to return to normal, and the hypertensive level of pressure decreased only slightly. In the chronic 1-KHT dogs, indomethacin did not lower plasma renin activity or mean arterial blood pressure unless plasma renin activity was elevated above the normal level. Also, indomethacin failed to alter renal function during the acute phase of 1-KHT but effective renal plasma flow fell during chronic 1-KHT. These results suggest that, in the dog, renal prostaglandins are involved in the pathogenesis of both acute 1-KHT and 2-KHT, whereas the role of renal prostaglandins in the regulation of arterial pressure appears to be negligible in chronic 1-KHT except during superimposed sodium depletion or severe hypertension. The data indicate that prostaglandins are involved in renovascular hypertension in the dog only under conditions where plasma renin activity is elevated. It is suggested that the release of renin after renal artery constriction is mediated by the vascular receptor that is at least partially independent of renal prostaglandin synthesis.
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PMID:Effects of indomethacin in dogs with acute and chronic renovascular hypertension. 701 3

The authors studied the effect of prostacycline and prostaglandins E2 and F2 alpha on the tonus of renal vessels of normotensive rats and rabbits, as well as on the noradrenalin action in the renal and lymph vessels of normotensive and spontaneously hypertensive rats. The effect of prostacycline and prostaglandin E2 proved to be dependent on the type of the animals: in rabbits they reduced, whereas in rats they increased renal perfusion pressure. Indomethacin reduced, while prostaglandin E2 restored the noradrenalin-induced pressor reaction in normotensive rats. In rats with spontaneous hypertension these effects were less pronounced. Prostaglandin F2 alpha increased the pressor effect of noradrenalin both in normotensive and in spontaneously hypertensive rats.
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PMID:[Effect of prostacyclin and prostaglandins E2 and F2 alpha on the vascular tone and reactivity of the kidneys and extremities]. 701 79


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