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1 Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA, USA
* To whom correspondence should be addressed. E-mail: mprieto{at}tulane.edu.
Angiotensin II (AngII)-infused rats exhibit increases in distal nephron renin expressed in principal cells of connecting tubules and collecting ducts. This study was performed to determine if the augmentation of distal nephron renin involves AngII type 1 (AT1)-receptor activation. Male Sprague-Dawley rats (200-220 g) were divided into 3 groups: 1) Sham-operated (n=8), AngII-infused (80 ng/min, 13 d, n=8), and AngII-infused plus AT1-receptor blocker (ARB), olmesartan (5 mg/d, n=8). AngII infusion increased systolic blood pressure (BP, 178±4 mmHg vs 122±1 mmHg; P<0.001) and suppressed plasma renin activity (PRA, 0.08±0.1 ngAngI.mL-1.h-1 vs 5.3±0.8 ngAngI.mL-1.h-1). ARB treatment prevented the increase in BP (113±6 mmHg) and led to increases in PRA (15.8±1.5 ngAngI.mL-1.h-1). Renin protein levels measured in the kidney medulla, to avoid contribution from JGA cells, were higher in AngII-infused rats (1.64±0.3 vs 1.00±0.1 densitometric units (DU) compared with Sham-operated rats; P<0.05) and ARB treatment prevented this increase (1.01±0.1). Likewise, renin immunoreactivity increased in medullary collecting ducts of Ang II-infused compared with Sham operated rats (2.5±0.3 vs 1.0±0.2 DU; P <0.001), which was also prevented by ARB (1.01±0.06). Renin qRT-PCR in AngII-infused rats showed higher mRNA levels in the kidney medulla compared with Sham-operated rats (5.5±2.3 vs 0.04±0.02 ratio to GAPDH mRNA levels; P<0.001); however, renin transcript levels were normalized in the ARB treated rats. These data demonstrate that the augmentation of distal nephron renin in AngII-infused hypertensive rats is AT1-receptor mediated. The augmented distal tubular renin may contribute to increased intratubular AngII levels and distal nephron sodium reabsorption in AngII-dependent hypertension.
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