Modification of atrial natriuretic peptide system in cold-induced hypertensive rats.

Kuichang Yuan, Xuanshun Jin, Woo Hyun Park, Jong Hun Kim, Byung-Hyun Park, Suhn Hee Kim

Index: Regul. Pept. 154(1-3) , 112-20, (2009)

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Abstract

Cold exposure induces hypertension and cardiac hypertrophy via sympathetic activation. The sympathetic nervous system is fundamentally important for the regulation of cardiac atrial natriuretic peptide (ANP) secretion. The present study aimed to define changes in ANP level with renal functions during cold exposure of rats. We also measured the direct effects of adrenergic stimulation on ANP secretion in cold-induced hypertensive rat atria. Sustained elevation of blood pressure and tachycardia were observed by 2-wk cold exposure. Cold exposure increased urine volume, UNaV, UKV and positive water balance. Atrial ANP content, its mRNA level, and plasma ANP concentration increased. Plasma norepinephrine level was increased but both alpha(1A)- and beta(1)-adrenoceptor (AR) mRNA levels in atrium were decreased. In isolated perfused atria from cold-exposed rats, basal ANP secretion increased and pulse pressure decreased. Phenylephrine (alpha(1)-AR agonist)-induced stimulation of ANP secretion, and isoproterenol (beta-AR agonist)-induced suppression of ANP secretion were significantly attenuated. These results suggest that an increased plasma and atrial ANP level by cold exposure may be a compensatory response to changes in hemodynamics and body fluid balance. The phenylephrine- and isoproterenol-induced attenuation of ANP secretion in cold-exposed rat atria may be due to the downregulation of alpha(1A)- and beta(1)-adrenoceptors mRNA levels.