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Elimination of pressure load via regional hypotension prevents the development of adaptive media increase in resistance vessels of spontaneously hypertensive rats.
In 3 week old spontaneously hypertensive rats (SHR) and normotensive control rats (NCR) the aorta was ligated distally to the renal arteries, lowering the blood pressure in the hindquarters some 30–50 per cent compared with “ordinary” NCR or SHR. 6–16 weeks later the hindquarters of an ordinary NCR were perfused simultaneously with those of an aorta‐ligated NCR or SHR in 20 paired experiments at constant flow with an oxygenated plasma substitute, from maximal dilatation to maximal constriction as induced by graded noradrenaline (NA) doses. Constructed “resistance curves” of the aorta‐ligated NCR and SHR hindquarters showed a 40–50 % decreased resistance at maximal dilatation with almost proportional decreases of the steepness of the dose‐response curve and of the maximal pressor response, when compared with ordinary NCR, while the threshold sensitivity to NA was the same as in unligated shamoperated NCR. The difference from unligated SHR was still more striking, yielding three separate sets of “resistance curves” each related to the pressure level present in the hindquarters during the months prior to the perfusion. The results indicate an adaptive structural change of the resistance vessels in the chronically hypotensive hindquarters with a media reduction and considerably increased vascular lumina. Thus, the elimination of the pressure load seems capable of completely preventing the development of the adaptive media increase that otherwise seems to occur in SHR. An altered pressure load, decreased or increased, evidently affects the design of the resistance vessels rapidly and this, in turn, will greatly contribute to the hemodynamic differences characterizing hypo‐ and hypertension as compared to normotension.
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Folkow et al. (1971) studied this question.
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