Why the study?
Does hexamethonium reduce arterial pressure and vascular resistance differently in conscious spontaneously hypertensive rats compared to normotensive controls?
Does hexamethonium reduce arterial pressure and vascular resistance differently in conscious spontaneously hypertensive rats compared to normotensive controls?
In conscious spontaneously hypertensive rats, elevated vascular resistance and arterial pressure are likely sustained by mechanisms other than neurally-derived vasoconstrictor tone.
Equivalent hexamethonium effects in SHR and WKY suggest non-neural mechanisms sustain hypertension; leaves open sympathetic contributions in conscious models.
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.
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Touw et al. (1980) studied this question.
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