Propranolol in doca hypertensive rats: Development of hypertension inhibited and pressor responsiveness enhanced

Buñag, Ruben D.

doi:10.1016/0014-2999(77)90038-3

Cited by 16 publications

(4 citation statements)

References 30 publications

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“…Another drug with selective but weak antihypertensive effects that could be centrally mediated is propranolol. 28 Because identical blood pressure levels can be produced in normotensive and DOCA hypertensive rats by cutting the spinal cord at the C6-C7 level, 23 but not by destroying the posterior hypothalamus, 11 sympathetic nerve hyperactivity may be occurring at sites on the neuraxis lower than the posterior hypothalamus. Thus, the apparent contradiction between enhanced pressor responsiveness to hypothalamic stimulation 10 on the one hand, and the lack of a greater hypotensive effect upon hypothalamic destruction 11 on the other, would be resolved.…”

Section: Discussionmentioning

confidence: 99%

Augmented sympathetic nerve activity and pressor responsiveness in DOCA hypertensive rats.

Takeda¹,

Buñag²

1980

Hypertension

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SUMMARY Spike potentials in abdominal sympatheticDenes were recorded together with aortic blood pressure before and during electrical stimulation of the posterior hypothalamus in urethane-anesthetized rats. Both the initial rate of sympathetic nerve firing and the subsequent acceleration produced by hypothalamic stimulation were higher in deoxycorticosterone acetate (DOCA) hypertensive than in normotensive rats. Pressor responsiveness was generally augmented, but responses to hypothalamic stimulation were increased far more than those to injected noreplnephrine. Vasodepression produced by blocking autonomlc ganglia pharmacologically with pentolinium was also more pronounced in DOCA hypertensive rats than in normotensive controls. These results support the conclusion that a centrally induced sympathetic hyperactivity is important for maintaining the blood pressure elevation in rats with established DOCA hypertension. conflicting but almost equally popular views now exist on whether sympathetic hyperactivity participates in causing deoxycorticosterone acetate (DOCA) hypertension. Supporting the belief that sympathetic hyperactivity is essential, the hypotension induced by combining adrenalectomy with chemical sympathectomy has been shown to result in identical blood pressure levels in adult normotensive and DOCA hypertensive rats. 1 Also, to restore blood pressure levels following splanchnicotomy during pentobarbital anesthesia, the splanchnic nerves had to be stimulated at much higher frequencies in DOCA hypertensive than in other rats. s Furthermore, destruction of central catecholaminergic neurons through intracerebroventricular injection of 6-hydroxydopamine prevents not only the elevation in tail-cuff systolic pressure 3 but also the attendant increase in plasma norepinephrine* in unanesthetized DOCA hypertensive rats. On the contrary, however, others have found DOCA hypertension either unaffected in adult rats Received January 22,1979; revision accepted September 17,1979. worse in neonates 79 after chemical sympathectomy. Observations that seem contradictory have also been made in our laboratory: DOCA hypertensive rats have an enhanced pressor responsiveness to hypothalamic stimulation, 10 yet their pressures fell only to the same levels as those of normotensive rats when the hypothalamus was destroyed. 11 In an attempt to find a logical explanation for this, we recorded sympathetic nerve activity directly before and during hypothalamic stimulation. To determine if the sympathetic overactivity thereby revealed would account for the elevation in blood pressure, we also measured vasodepression occurring after pentoliniuminduced ganglion blockade. MethodsFemale Sprague-Dawley rats, 3 weeks old, were purchased from Charles River Breeding Laboratories (Wilmington, MA). Soon after arrival, all were anesthetized with sodium amobarbital (8 mg/100 g i.p.) and their left kidneys removed. Silicon rubber molds containing DOCA (200 mg/kg) were implanted subcutaneously in eight rats, according to the method of Ormsbee ...

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Section: Discussionmentioning

confidence: 99%

Augmented sympathetic nerve activity and pressor responsiveness in DOCA hypertensive rats.

Takeda¹,

Buñag²

1980

Hypertension

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“…In mature spontaneously hypertensive rats, propranolol has been reported to lower (Roba, Lambelin & de Schaepdryver, 1972) or to have no effect on (Forman & Mulrow, 1974, Buniag, 1977 systolic BP, and to lower (Garvey & Ram, 1975) to raise (Nakao, Kato & Takagi, 1975) or to have no effect on (Weiss, Lundgren & Folkow, 1974;Conway, Darwin Hilditch, Loveday & Reeves, 1975) mean arterial BP. Furthermore, it has been found that pretreatment with propranolol may either not affect (Frohlich & Pfeffer, 1975) or may prevent (Weiss et al, 1975) the development of the spontaneous hypertension.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, it has been found that pretreatment with propranolol may either not affect (Frohlich & Pfeffer, 1975) or may prevent (Weiss et al, 1975) the development of the spontaneous hypertension. There are reports of either a reduction (Dusting & Rand, 1974, Buniag, 1977 or no change (Farmer & Levy, 1968) in the systolic BP of deoxycorticosterone acetate (DOCA)-saline hypertensive rats, and the mean arterial BP of such hypertensive animals has been reported not to change after propranolol treatment (Conway et al, 1975). However, it is generally agreed 0007-1188/79/020205-09 $01.00 that pre-loading with propranolol does prevent the development of hypertension in young rats with DOCA implants given saline to drink (Conway et al, 1975;Bufiag, 1977).…”

Section: Introductionmentioning

confidence: 99%

PREVENTION AND REVERSAL OF ISOLATION-INDUCED SYSTOLIC ARTERIAL HYPERTENSION IN RATS BY TREATMENT WITH Β-Adrenoceptor ANTAGONISTS

Bennett

Gardiner

1979

British Journal of Pharmacology

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1 Rats were made hypertensive by 5 days of continuous isolation in glass metabolic cages; in the text 'hypertensive' means having a systolic blood pressure greater than 145 mmHg.2 Daily intraperitoneal injections of either propranolol (5 mg/kg) or atenolol (5 mg/kg) reduced systolic blood pressure within 3 days and the systolic blood pressure remained low provided that the treatment was continued. 3 Treatment with metoprolol also lowered the systolic blood pressure of isolated rats but only when a larger dose (10 mg/kg) was given. 4 Systolic blood pressure returned to hypertensive levels following withdrawal of treatment after 15 days of isolation. However, following cessation of treatment after 27 days of isolation, the systolic blood pressure did not rise.5 Rats given propranolol in the drinking water (intake equivalent to a daily dose of 5 mg/kg) before and during isolation did not develop hypertension. 6 The possibility that suppression of sympathetic function by the fl-adrenoceptor antagonists was responsible for these changes is discussed.

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“…A test dose of 1.6 mg/100g was used routinely since the bradycardia it produces had previ ously been shown to be maximal and unaf fected by further increases in dose (5). Unlike mecamylamine, propranolol caused consistent bradycardia but affected systolic pressure ir regularly.…”

Section: Sympathetic Hyperactivity In Enovid-treated Renal Hypertensimentioning

confidence: 99%

Does Oral Contraceptive (Enovid) Treatment Enhance Renal Hypertension in Rats by Inducing Sympathetic Hyperactivity?

Buñag¹

1980

Pharmacology

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One-kidney renal hypertension was induced in rats that had been given Enovid or corn oil by daily gavage for 5 weeks, and treatment was then continued postoperatively for 10 weeks more. Systolic pressures began to rise almost immediately after hypertension was induced, and from the 4th postoperative week on, the pressure elevation was consistently more pronounced in Enovid-treated than in corn oil-treated rats. When autonomic ganglia were subsequently blocked with mecamylamine, the ensuing blood pressure fall was invariably larger in Enovid-treated than in corn oil-treated rats. In contrast, responses to β-adrenergic blockade with propranolol were equivocal; heart rates fell while systolic pressures rose slightly to about the same extent in both groups. The larger hypotensive response to ganglion blockade in Enovid-treated rats is in accord with the interpretation that Enovid treatment augments development of renal hypertension by increasing sympathetic vasomotor tone.

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Propranolol in doca hypertensive rats: Development of hypertension inhibited and pressor responsiveness enhanced

Cited by 16 publications

References 30 publications

Augmented sympathetic nerve activity and pressor responsiveness in DOCA hypertensive rats.

Augmented sympathetic nerve activity and pressor responsiveness in DOCA hypertensive rats.

PREVENTION AND REVERSAL OF ISOLATION-INDUCED SYSTOLIC ARTERIAL HYPERTENSION IN RATS BY TREATMENT WITH Β-Adrenoceptor ANTAGONISTS

Does Oral Contraceptive (Enovid) Treatment Enhance Renal Hypertension in Rats by Inducing Sympathetic Hyperactivity?

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