RESUMEN
Se utilizó la saralasina, un bloqueador competitivo de la angiotensina II, con el propósito de incrementar el flujo sanguíneo renal y la tasa de filtración glomerular, para estudiar sus posibles consecuencias tubulares y sobre la presión arterial. Fueron divididas 40 ratas de la línea Wistar, inicialmente normotensas, en 4 grupos: saralasina, supresión, grupos controles corrieron paralelos. Se les realizaron a todos mediciones de variables hemodinámicas sistémicas y renales, así como morfométricas del riñón. Los resultados apoyaron la hipótesis de la participación de la hiperfunción tubular en la génesis de la hipertensión arterial primaria y propusieron un nuevo modelo de hipertensión arterial experimental en ratas(AU)
Asunto(s)
Animales , Ratas , Hipertensión , Angiotensina II , Animales de Laboratorio , Riñón , Saralasina/antagonistas & inhibidoresRESUMEN
OBJECTIVE: Our null hypothesis was that the angiotensin II antagonist saralasin does not reduce the number of ovulations in the rat ovarian perfusion model. STUDY DESIGN: Ovaries from pregnant mare's serum gonadotropin-stimulated immature rats were perfused with nutrient media to which luteinizing hormone and 3-isobutyl-1-methylxanthine had been added to induce ovulation. Test perfusions were treated with saralasin 1 mumol/L (n = 0.5) and compared with controls (n = 5) with the Student t test. Perfusions with both saralasin and angiotensin II and dose-response evaluations were performed. RESULTS: Saralasin-treated ovulations were 6.6 +/- 1.3 (mean + SEM) compared with 18.6 +/- 3.9, p < 0.02. The effects of saralasin could be reversed with the addition of an equimolar amount of angiotensin II. Dose-response evaluations showed a progressive inhibition of ovulation at 10(-8) to 10(-6) mol/L. CONCLUSION: The angiotensin II antagonist saralasin inhibits ovulation in a dose-dependent fashion; this effect is canceled by the addition of equimolar concentrations of angiotensin II.
Asunto(s)
Angiotensina II/farmacología , Ovario/efectos de los fármacos , Ovulación/efectos de los fármacos , Saralasina/farmacología , Animales , Relación Dosis-Respuesta a Droga , Femenino , Gonadotropinas Equinas/administración & dosificación , Perfusión , Ratas , Ratas Sprague-Dawley , Saralasina/antagonistas & inhibidoresAsunto(s)
Aldosterona/sangre , Angiotensina II/análogos & derivados , Coartación Aórtica/cirugía , Natriuresis , Renina/sangre , Saralasina/antagonistas & inhibidores , Adolescente , Coartación Aórtica/sangre , Niño , Humanos , Hipertensión/etiología , Periodo Posoperatorio , Sistema Renina-AngiotensinaRESUMEN
Under inactin anesthesia, intravenous infusion of [Sar1,Thr8]angiotensin II produced a hypotensive effect in young spontaneously hypertensive rats (SHR) treated with furosemide and in mature SH rats fed a low-sodium diet. The angiotensin antagonist also lowered blood pressure of young and mature SH rats receiving a normal diet. Deoxycorticosterone acetate (DOCA) plus saline reversed the hypotensive effect of [Saru,Thr8]angiotensin II in young SH rats, but did not do so in mature SH rats. Plasma renin activity (PRA) was not significantly changed by anesthesia. Furosemide or the low-sodium diet significantly increased PRA in young and mature SH rats. In contrast, DOCA plus saline significantly reduced PRA in both young and mature SH rats. However, there was no correlation between PRA and the action of the angiotensin II antagonist. These data suggest that the renin-angiotensin system is involved in genetic hypertension.
Asunto(s)
Angiotensina II/análogos & derivados , Presión Sanguínea/efectos de los fármacos , Hipertensión/fisiopatología , Saralasina/farmacología , Envejecimiento , Animales , Desoxicorticosterona/farmacología , Dieta Hiposódica , Hipertensión/genética , Hipertensión/orina , Infusiones Parenterales , Ratas , Renina/sangre , Saralasina/antagonistas & inhibidores , Sodio/orinaAsunto(s)
Angiotensina II/análogos & derivados , Angiotensina II/metabolismo , Hipertensión Renal/metabolismo , Saralasina/farmacología , Glándulas Suprarrenales/efectos de los fármacos , Aldosterona/metabolismo , Animales , Aorta/efectos de los fármacos , Colon/efectos de los fármacos , Corazón/efectos de los fármacos , Hemodinámica/efectos de los fármacos , Humanos , Hipertensión Renal/tratamiento farmacológico , Técnicas In Vitro , Pulmón/efectos de los fármacos , Renina/sangre , Saralasina/antagonistas & inhibidores , Saralasina/uso terapéutico , Estómago/efectos de los fármacos , Sed/efectos de los fármacosRESUMEN
Saralasin, an angiotensin antagonist, was used to study the role of renin-angiotensin in the vasodilator-beta-blocker drug interaction in hypertensive subjects. Plasma renin activity was elevated by withdrawal of propranolol in seven patients using minoxidil and propranolol. After propranolol withdrawal, saralasin caused hypotension (100/60 mm Hg or less) in five. Propranolol lowered blood pressure and plasma renin activity and diminished the hypotensive response to saralasin. Saralasin induced renin release in all patients, an effect blocked by propranolol. We conclude that angiotensin can be the major determinant of blood pressure in vasodilator-drug treated patients, that propranolol lowering of blood pressure in this vasodilator-beta-blocker drug interaction is related to suppression of renin release, and that the angiotensin feed-back-suppression mechanism for inhibiting renin release in functionally located proximal to beta-adrenergic receptors mediating renin release.