Why the study?
The vascular amplifier in hypertension arises from structural changes in resistance arteries, prompting estimation of the amplifier hypertensive:normotensive ratio in the renal bed versus the total peripheral bed.
Does the renal vascular resistance amplifier in hypertensive rabbits differ from normotensive rabbits during vasoconstrictor and vasodilator stimuli?
Does the renal vascular resistance amplifier in hypertensive rabbits differ from normotensive rabbits during vasoconstrictor and vasodilator stimuli?
The renal resistance amplifier in renal wrap hypertension with neurohumoral block is consistent with the total peripheral resistance amplifier, reflecting structural remodeling in the renal vascular bed.
Answers are grounded in this paper and cite their sources.
Rabbit renal H:N resistance amplifier (~1.7) matches systemic; leaves open structural remodelling's role in human hypertension.
OBJECTIVES: The vascular amplifier in hypertension is a result of structural changes in resistance arteries. We estimated the vascular amplifier hypertensive:normotensive (H:N) ratio in the renal bed compared with the total peripheral bed in conscious rabbits during infusion of vasoconstrictor and vasodilator stimuli. METHODS: Rabbits were subjected to bilateral renal cellophane wrap or sham operation. A perivascular ultrasonic flow probe was implanted on the left renal artery to measure renal blood flow. A catheter was inserted into the thoracic aorta for agonist administration. Blood pressure, heart rate and renal blood flow were measured on three separate days in conscious rabbits with intact effectors, ganglionic block or neurohumoral block. Dose-response curves were constructed to intra-arterial infusion of noradrenaline, angiotensin II, adenosine and acetylcholine. RESULTS: Resting renal vascular resistance in hypertensive rabbits was markedly decreased by ganglionic block and further by neurohumoral block. With effectors intact, ganglionic block or neurohumoral block, the H:N ratio for renal vascular resistance was 2.32, 1.72 or 1.72, respectively. The ratio was generally maintained during the infusion of constrictor and dilator drugs although distortions occurred at higher concentrations of constrictor or dilator drugs. CONCLUSIONS: Estimation of the renal resistance amplifier in renal wrap hypertension with neurohumoral block accords with our earlier estimates of the total peripheral resistance amplifier (1.79). This vascular resistance amplifier is consistent with a decrease in internal radius through structural remodelling in the renal vascular bed as is reflected in the total arterial circulation in hypertension.
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Khammy et al. (2020) studied this question.
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