Angiotensin II acts as vasoconstrictor via AT1 and as a vasodilator via AT2 receptors. Selective ligands of both receptor types are needed to study their relative importance or possible interaction in the control of normal or elevated arterial blood pressure (BP); the knowledge of the role of AT2 is still limited. In this study effects of a newly synthetized (A. Lipkowski) tripeptide AT2 agonist (LKP) on BP and intrarenal haemodynamics (renal artery Transonic probe, RBF; cortical-, outer- and inner medullary laser-Doppler fluxes, CBF, OMBF, IMBF) were determined in anaesthetised Wistar rats, receiving background intravenous infusion of norepinephrine (NE) which raised BP to 130±2 mmHg and in non-pretreated spontaneously hypertensive rats (SHR). LKP infusion (120 µg/kg/h i.v.) decreased BP (-4%, p<0.01), which was associated with a 9% increases in OMBF (p<0.05) and IMBF (NS) in Wistar rats. Although NE-induced hypertension was expected to inhibit endogenous angiotensin II synthesis, additional AT1 inhibition (losartan, 1 mg/kg i.v.) further decreased BP and increased OMBF, and tended to increase RBF. In SHR LKP infusion tended to decrease BP (-3%), which was associated with nonsignificant increase in RBF and IMBF. These changes were augmented by AT1 inhibition (losartan) and reach statistical significance. The findings indicate that the levels of AT1 and AT2 activity can independently influence arterial pressure in acutely hypertensive rats. A striking association of BP decrease with an increase in medullary blood flow suggests that perfusion of the renal medulla has a direct causative role in the control of arterial pressure. Acknowledgements. We are greatly indebted to Adamed Company, Sp. z o.o. (Pieńków, Poland) for providing us with losartan. Supported by the Polish Ministry of Science and Higher Education (grant No. N N 401225634).
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.