Angiotensin II and catecholamines interaction in short-term low protein feeding

Benabe, Julio E.; Fernández-Repollet, Emma; Tapia, Edilia; Chuying Luo; Martinez-Maldonado, Manuel
August 1993
Kidney International;Aug1993, Vol. 44 Issue 2, p285
Academic Journal
Renal and systemic hemodynamic responses to an α-adrenergic agonist (norepinephrine, NE) and an a-adrenergic antagonist (phentolamine, PHEN) were studied in weanling rats pair-fed isocaloric diets containing either normal (NP, 23%) or low (LP, 6%) protein. Mean arterial pressure (MAP) rose less with NE and fell more with PHEN in LP than in NP. Plasma NE and epinephrine (E; 46 ± 5 and 51 ± 4 ng/ml) were higher in LP than in NP (26 ± 3 and 39 ± 3 ng/ml). These could not be attributed to changes in red cell mass nor the volumes of plasma, extracellular, or interstitial fluid in LP versus NP. Plasma angiotensin II (Ang II): renin (PRA), and aldosterone (PA) were lower in LP than in NP. An increased number without changes in affinity of glomerular Ang II receptors was found in LP compared to NP, while α1- and α2-adrenergic receptors were down-regulated in LP as compared to NP without changes in affinity for the am receptor but with an increase in renal α2 receptor affinity. LP (vs. NP) decreased GFR and RPF, and increased renal vascular resistance (RVR). NE decreased RPF equally in NP versus LP but raised RVR approximately twofold in NP versus LP. PHEN decreased RPF and increased RVR less in LP than in NP. Moreover, PHEN increased renal renin content approximately seven-fold over the basal NP values. Exogenous Ang II increased RVR and lowered RPF more in LP than in NP. Enalapril abolished all the hemodynamic changes of LP and restored the systemic response to NE. These findings are evidence that short periods of protein deprivation lead to systemic and local (intrarenal) alterations in adrenergic state and the renin-angiotensin system, and that these two are principally responsible for the adaptive hemodynamic changes observed. Dietary protein plays a significant role in the hormonal regulation of intrarenal hemodynamics.


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