Why the study?
Earlier studies undermined the view that renal medullary blood flow controls arterial pressure, prompting examination of its role in normotensive, acutely elevated, and hypertensive rats.
Does a 4-hour selective increase in renal medullary blood flow via bradykinin infusion reduce mean arterial pressure in normotensive and hypertensive rats?
Does a 4-hour selective increase in renal medullary blood flow via bradykinin infusion reduce mean arterial pressure in normotensive and hypertensive rats?
Selective hyperperfusion of the renal medulla for 4 hours does not alter mean arterial pressure in normotensive or hypertensive rat models, providing further evidence against the view that medullary blood flow is a critical short-term determinant of blood pressure.
Questions MBF modulation for MAP control; challenges consensus in rat models and leaves open human relevance.
Earlier evidence from studies of rat hypertension models undermines the widespread view that the rate of renal medullary blood flow (MBF) is critical in control of arterial pressure (MAP). Here, we examined the role of MBF in rats that were normotensive, with modest short-lasting pressure elevation, or with overt established hypertension. The groups studied were anaesthetised Sprague-Dawley rats: (1) normotensive, (2) with acute i.v. norepinephrine-induced MAP elevation, and (3) with hypertension induced by unilateral nephrectomy followed by administration of deoxycorticosterone-acetate (DOCA) and 1% NaCl drinking fluid for 3 weeks. MBF was measured (laser-Doppler probe) and selectively increased using 4-h renal medullary infusion of bradykinin. MAP, renal excretion parameters and post-experiment medullary tissue osmolality and sodium concentration were determined. In the three experimental groups, baseline MAP was 117, 151 and 171 mmHg, respectively. Intramedullary bradykinin increased MBF by 45%, 65% and 70%, respectively, but this was not associated with a change in MAP. In normotensive rats a significant decrease in medullary tissue sodium was seen. The intramedullary bradykinin specifically increased renal excretion of water, sodium and total solutes in norepinephrine-treated rats but not in the two other groups. As previously shown in models of rat hypertension, in the normotensive rats and those with acute mild pressure elevation (resembling labile borderline human hypertension), 4-h renal medullary hyperperfusion failed to decrease MAP. Nor did it decrease in DOCA-salt model mimicking low-renin human hypertension. Evidently, within the 4-h observation, medullary perfusion was not a critical determinant of MAP in normotensive and hypertensive rats.
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Bądzyńska et al. (2021) studied this question.
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