Contribution of the sympathetic nervous system to vascular resistance in conscious young and adult spontaneously hypertensive rats.

Although evidence exists for exaggerated sympathetic nervous system activity in spontaneously hypertensive rats (SHR), there are no studies in conscious animals that directly demonstrate that this increased activity is functionally involved in the elevated vascular resistance of these animals. In our present study, 8-week-old and 13-week-old SHR and Wistar Kyoto controls (WKY) were chronically instrumented with arterial and venous catheters and miniaturized pulsed Doppler flow probes on the renal and mesenteric arteries and lower abdominal aorta. While the rats were conscious and unrestrained, hexamethonium was administered intravenously to block sympathetic nervous system transmission. Prior to hexamethonium, the mean arterial pressure of young SHR and WKY averaged 123 plus or minus 5 and 109 plus or minus 4 mm Hg respectively (p smaller than 0.05), while adult SHR and WKY averaged 159 plus or minus 7 and 128 plus or minus 3 mm Hg respectively (p smaller than 0.05). Hexamethonium produced an equivalent fall in arterial pressure of young SHR (-32%) and WKY (-30%) and adult SHR (-39%) and WKY (-41%). Vascular resistance was reduced by hexamethonium in the kidney, gut, and hindquarters, but the percent changes were not significant between SHR and WKY. These data suggest that, in both young and adult SHR, vascular resistance and arterial pressure are sustained at elevated levels by some other mechanism than neurally-derived vasoconstrictor tone.

Factors influencing the altered pain perception in the spontaneously hypertensive rat.

Recent studies have demonstrated a hypoalgesia in hypertensive subjects. This study reports and evaluates factors responsible for the expression of the hypoalgesic behavior demonstrated by genetically hypertensive rats of the Okamoto-Aoki strain (SHR) as compared to normotensive age-matched Wistar-Kyoto rats (WKY). Analgesiometric assays were conducted by the hot plate method. SHR's hypoalgesic behavior was reversed by subcutaneously administered naloxone. The intravenous administration of naloxone did not alter arterial pressure or heart rate in either SHR or WKY. Subcutaneous administration of the peripherally acting ganglionic blocker hexamethonium bromide at a dose which lowered mean arterial blood pressure and thus decreased tonic baroreceptor stimulation, concomitantly reversed the SHR hypoalgesic behavior and induced a hyperalgesia in WKY. Denervation of the sino-aortic baroreceptors failed to alter the hypoalgesic behavior demonstrated by SHR. Denervation of the right vagal nerve trunk with associated cardiopulmonary baroreceptor afferents resulted in a reduction of the SHR hypoalgesic behavior and produced a hyperalgesic behavior in WKY as compared to age-matched sham operated controls over a 4 week period. These data suggest a possible physiological role for vagal afferent systems in the concomitant regulation of resting arterial blood pressure and responsiveness to aversive environmental stimuli. A discussion of the interaction between blood pressure and pain regulatory systems as potential substrates associated with the onset and maintenance of hypertension is provided.