Search PubMed⌕ Search

Biomedical subjects

E N Bush

Publications and source records attributed to E N Bush.

23 records · Page 2Linked to original sources
PubMed1984

Contribution of beta-adrenergic receptor mediated renin release to the maintenance of blood pressure during nitroprusside infusion in conscious rats.

The extent to which beta-adrenergic receptor mediated renin release contributes to the maintenance of blood pressure during hypotension induced by sodium nitroprusside (SNP, 40 micrograms/kg/min for 30 min) was assessed in conscious Wistar rats fitted with chronic aortic and vena caval catheters. Propranolol, (1.5 mg/kg, i.v.), reduced the basal level of plasma renin activity (PRA) in control rats from 4.4 +/- 0.4 to 2.4 +/- 0.4 ng angiotensin I/ml/min (p less than .05) and decreased PRA obtained during SNP infusion from 35.3 +/- 6.6 to 16.7 +/- 2.2 ng angiotensin I/ml/min (p less than .01). Despite the reduced PRA, the hypotensive response to SNP was not enhanced after propranolol. Treatment of these animals with captopril in order to block the actions of the remaining non-beta-receptor released renin, resulted in augmentation of the SNP hypotension. Captopril also potentiated SNP hypotension in rats that had not received propranolol. The addition of propranolol to the captopril treated rats produced no further change in SNP hypotension. The results of this study indicate that beta-receptor-mediated and beta-receptor-independent mechanisms contribute to the renin released during SNP hypotension. However, if the beta-receptor-mediated component alone is blocked, the remaining renin secretion is adequate to maintain blood pressure during SNP infusion.

Animals↗
PubMed1983

Effects of dietary sodium restriction on heart rate control in rats.

The effects of dietary sodium restriction on heart rate control were evaluated in male Wistar rats maintained for 4 wk on a low- (22 meq/kg diet) or standard (141 meq/kg diet) sodium diet. In conscious low-sodium rats, atropine produced heart rate increases greater than in standard sodium animals, indicating that basal parasympathetic tone was elevated. Sodium restriction did not affect basal sympathetic tone, since similar reductions in heart rate were produced by propranolol in both dietary groups. However, sympathetically mediated tachycardic responses to sodium nitroprusside were augmented in low-sodium rats. This enhancement of sympathetic function was also observed in low-sodium animals after pithing. The increases in heart rate produced by spinal sympathetic stimulation were significantly accentuated; whereas, responses to norepinephrine were not affected by the diets. This finding is in agreement with the observation that the chronotropic responses elicited by isoproterenol in isolated atria were not altered. When neuronal influences on heart rate were blocked by combined administration of atropine and propranolol or chlorisondamine in conscious rats, the underlying intrinsic cardiac rate was found to be significantly higher in low-sodium rats. In summary, the present study identifies three effects of sodium restriction on heart rate control in the rat: 1) basal parasympathetic tone is increased, 2) heart rate responses to sympathetic activation are enhanced, and 3) the intrinsic cardiac rate is elevated.

Animals↗
PubMed1983

Reduced sympathetic responsiveness resulting from a high dietary sodium intake in the rat.

The effects of a high sodium diet on sympathetic nervous function were evaluated in normotensive male Wistar rats maintained on a standard (141 mEq/kg) or high (1400 mEq/kg) sodium chow for 4 weeks. No differences were observed in the blood pressures of conscious catheterized rats on the two diets; however, heart rates were significantly lower in rats on the high sodium intake. Hypotensive responses produced in these animals by one minute intravenous infusions of sodium nitroprusside were greater in rats on the high sodium diet, whereas, reflex tachycardia was similar. In pithed rats on either diet, basal blood pressures and heart rates were similar. In contrast, blood pressure responses to electrical stimulation of the spinal sympathetic outflow were significantly attenuated in the high sodium rats but the tachycardic responses were unaltered. In addition, norepinephrine induced blood pressure and heart rate increases were not different between the diets. Similarly, the sensitivity of isolated atria to isoproterenol was not affected by dietary sodium, nor were the responses of isolated aortic strips to phenylephrine altered. The results of this investigation indicate that a chronic high sodium intake may result in an attenuation of vascular sympathetic function.

Animals↗
PubMedDate not supplied

Adrenergic and dopaminergic properties of dopamine sulfoconjugates.

UNLABELLED: The 3- and 4-sulfate esters of dopamine (DA-3-SO4 and DA-4-SO4, respectively), the two main metabolites of DA, were evaluated for potential intrinsic or indirect catecholaminergic activities. Both compounds lacked any appreciable affinities for alpha 1, alpha 2, beta 1, beta 2 and DA-2 receptors. In the superfused [3H]norepinephrine-preloaded dog saphenous vein, both dopamine sulfates were devoid of any intrinsic inhibitory activity such as observed with dopamine pre- and postsynaptically. In addition, they did not displace the labeled vesicular neurotransmitter as did dopamine. In anesthetized dogs the two compounds failed to stimulate either the dopaminergic receptors (DA-1) of mesenteric vascular beds or the adrenergic receptors mediating the vasodilatory and pressor responses to dopamine. CONCLUSION: In our experimental conditions DA-3-SO4 and DA-4-SO4, the products of dopamine sulfoconjugation, lacked any demonstrable intrinsic affinity and/or efficacy on the dopaminergic and adrenergic receptors directly or indirectly through their metabolic transformation or through displacement of endogenous neurotransmitter.

Animals↗