Development of hypertension induced by subpressor infusion of angiotensin II: Role of sensory nerves

Abstract

Long-term administration of a subpressor dose of angiotensin II (Ang II) leads to pressor hyperresponsiveness and slow development of hypertension. Our preliminary data show that mRNA expression for calcitonin-gene related peptide in dorsal root ganglia was significantly increased by subpressor infusion of Ang II. To determine the role of sensory nerves in the development of hypertension induced by subpressor infusion of Ang II, newborn Wistar rats were given 50 mg/kg SC capsaicin on the 1st and 2nd days of life. After the weaning period, male rats were divided into 4 groups and subjected to the following treatments for 2 weeks: capsaicin+Ang II (150 ng · kg-1 · min-1 SC by osmotic pumps, CAP-AII), capsaicin+vehicle (CAP), control+Ang II (CON-AII), and control+vehicle (CON). The results show that mean arterial pressure was significantly elevated in both Ang II-infused rats compared with non-Ang II-treated rats (P<0.05), and it was higher in CAP-AII than in CON-AII rats (P<0.05). The 24-hour urinary and sodium excretions were lower in CAP-AII than in CON-AII, CAP, and CON rats (P<0.05). These data demonstrated that sensory denervation exacerbates the development of hypertension and impairs renal excretory function when a subpressor dose of Ang II is given. These results indicate that activation of sensory nerves, either by Ang II (or by other hormonal or hemodynamic factors, plays a compensatory role in promoting urine and sodium excretion and attenuating elevated blood pressure initiated by Ang II.