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A role for Gαi 2 proteins in the acute neural control of blood pressure.
Author(s) -
Carmichael Casey Yumi,
Wainford Richard D
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.927.9
Subject(s) - baroreflex , sodium nitroprusside , phenylephrine , blood pressure , chemistry , bolus (digestion) , endocrinology , medicine , sodium , mean arterial pressure , endogeny , homeostasis , anesthesia , heart rate , nitric oxide , organic chemistry
Aim We have demonstrated hypertension mediated by failure to upregulate hypothalamic paraventricular nucleus Gαi 2 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 Gαi 2 proteins in the neural control of blood pressure in response to an acute pharmacological and physiological challenge. Methods Naïve and 24hr ICV Gαi 2 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). Results 24h Gαi 2 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. Gαi 2 treated animals (Naïve + 3M NaCl ΔHR=−79±15 bpm vs . Gαi 2 + 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 . Gαi 2 + 3M NaCl MAP 149±3 mmHg). In naïve rats, MAP returned to baseline by 100 min whereas Gαi 2 animals remained significantly elevated for 120 min (P<0.05). Conclusion Endogenous Gαi 2 proteins are involved in neural control of HR and MAP during an acute sodium challenge. These data suggest brain Gαi 2 signal transduction is required to mediate sodium‐sensitive neural responses to maintain physiologically appropriate blood pressure regulation.