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Pressor Hyperreactivity to Stress Corresponds to Greater Vasoconstriction and Sympathetic Responsiveness and is Prevented by Renal Denervation
Author(s) -
Knuepfer Mark M,
Burris Sarah K,
Perry Jeffrey L
Publication year - 2017
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.31.1_supplement.717.7
Subject(s) - cold pressor test , medicine , denervation , blood pressure , vasoconstriction , reflex , heart rate , sympathetic nervous system , vascular resistance , endocrinology , baroreflex , hemodynamics , anesthesia , cardiology
Renal denervation is effective in reducing arterial pressure in some patients with resistant hypertension. The cardiovascular reactivity hypothesis proposes that enhanced pressor responsiveness to stressful stimuli in humans predicts predisposition to develop hypertension and cardiovascular disease. Clinical studies have suggested, but not always verified, that pressor hyperreactivity correlates with greater muscle sympathetic nerve activity (SNA) responses. Our laboratory has shown that outbred Sprague‐Dawley male rats have variable pressor responsiveness to acute stress (air jet or cold water exposure). We reported that rats with larger acute pressor responses to stress lose this greater sensitivity after renal denervation or selective deafferentation using intrarenal capsaicin administration. We hypothesized that greater pressor sensitivity in the rat model reflects greater sympathetic responsiveness and dependence on renal sensory input to promote sympathetic tone. Rats were instrumented for recording arterial pressure (AP), heart rate, ascending aortic blood flow as a measure of cardiac output and both renal and adrenal SNA. After recovery, rats were tested with a brief air jet (1 sec, 30 psi) to the face, and with cold water exposure (1 cm deep for 1 min) while recording hemodynamic and sympathetic variables. As expected, both renal and adrenal SNA were significantly increased, particularly during the initial few seconds after onset of the stressor exposure. Rats were separated into those with larger and those with smaller pressor responses (32.5 ±1.5 vs 23.6±0.9 mmHg) to cold stress. The differences correlated with greater increases in calculated systemic vascular resistance (44.1±3.3 vs 33.4±2.4%). They also correlated with greater increases in renal SNA (660±54 vs 488±32%, p<0.013) and greater increases in adrenal SNA (713±99 vs 450±48%, p<0.034). As noted, the differences in hemodynamic responses were prevented by renal denervation in a separate group of rats. After renal denervation, all rats had similar pressor and vasoconstrictor responses to cold water stress. We conclude that rats have variable pressor responsiveness that is correlated with greater renal and adrenal SNA. We predict that this model may reveal a means to study sympathetic hyperreactivity and how this is related to predisposition to develop cardiovascular disease. In the future, we will verify that SNA responses are also normalized by renal denervation. Support or Funding Information Supported by USPHS DA13256 and St. Louis University.