RESUMEN
The pressor interactions between angiotensin II and norepinephrine were investigated in conscious New Zealand white rabbits receiving a low sodium diet. Angiotensin II was administered continuously by intraperitoneal osmotic pumps in a subpressor dose so as to avoid the potentially confounding effects of experimentally-induced hypertension. Norepinephrine challenges were given as a series of graded intravenous boluses. During the 3 days of study the baseline blood pressure in the angiotensin-treated rabbits (n=10) did not differ from that in controls (n=10) whose intraperitoneal pumps contained only diluent. After 24 hours the systolic and diastolic blood pressure responses to norepinephrine in the angiotensin-treated group were, on average, 45% and 30% higher than in the controls; after 72 hours, they were 46% and 34% higher. Although the pressor amplitudes were increased by angiotensin II, they were not prolonged. Thus, facilitation by the subpressor angiotensin II of the blood pressure responses to norepinephrine did not seem dependent upon alterations in endogenous sympathetic mechanisms or the uptake of norepinephrine; nor could it be explained by sodium retention. It is possible that angiotensin II exhibits its effect by enhancing contractile responsiveness to norepinephrine at the postreceptor level.
Asunto(s)
Angiotensina II/farmacología , Presión Sanguínea/efectos de los fármacos , Norepinefrina/farmacología , Animales , Peso Corporal/efectos de los fármacos , Interacciones Farmacológicas , Frecuencia Cardíaca/efectos de los fármacos , Masculino , Conejos , Renina/sangreRESUMEN
Insulin hypoglycemia or epinephrine release may lead to adverse increases in blood pressure in the presence of non-cardioselective beta-blockers. However, increases in blood pressure have not been observed in beta-blocker treated patients during physical exercise, handgrip tests, or during infusions with the alpha-adrenergic agonist, phenylephrine. In this study we have further evaluated the role of adrenergic stimuli in the etiology of these responses of blood pressure during beta-blocker therapy. These data do not support a direct role for beta 2 receptors or norepinephrine in pressor responses observed during beta-blocker therapy. Blockade of beta 1 receptors or, more likely, a facilitating effect of propranolol upon the alpha-adrenergic receptors might explain the enhanced pressor responses found after administration of the alpha-adrenergic agonist, phenylephrine. However, high doses of phenylephrine seem needed to elicit such pressor responses.