A role for Gαi2 proteins in the acute neural control of blood pressure.

Abstract

AimWe have demonstrated hypertension mediated by failure to upregulate hypothalamic paraventricular nucleus Gαi2 proteins in rats fed a high salt diet, but the role of this mechanism is unknown in acute settings. We examined the effect of central Gαi2 proteins in the neural control of blood pressure in response to an acute pharmacological and physiological challenge.MethodsNaïve and 24hr ICV Gαi2 oligodeoxynucleotide (ODN; 25μg/5μl)‐pretreated conscious Sprague‐Dawley rats were continuously monitored for changes in HR and MAP in response to intravenous (IV) infusion of phenylephrine and sodium nitroprusside or 3M NaCl IV bolus (0.14 ml/100g). To determine cardiac baroreflex relationships, MAP was slowly raised to ~175 mmHg using phenylephrine and lowered to ~50 mmHg using sodium nitroprusside (N=8/gp).Results24h Gαi2 ODN pretreatment did not affect the cardiac baroreflex response. In response to IV sodium, peak changes in HR were significantly greater in naïve animals vs. Gαi2 treated animals (Naïve + 3M NaCl ΔHR=−79±15 bpm vs. Gαi2 + 3M NaCl ΔHR=−59±12 bpm; P<0.05). We observed no difference in peak MAP post‐IV NaCl between groups (Naïve + 3M NaCl MAP 147±4 mmHg vs. Gαi2 + 3M NaCl MAP 149±3 mmHg). In naïve rats, MAP returned to baseline by 100 min whereas Gαi2 animals remained significantly elevated for 120 min (P<0.05).ConclusionEndogenous Gαi2 proteins are involved in neural control of HR and MAP during an acute sodium challenge. These data suggest brain Gαi2 signal transduction is required to mediate sodium‐sensitive neural responses to maintain physiologically appropriate blood pressure regulation.