Long-term renal neuroadrenergic hypertension alters renal vascular reactivity

Sustained renal neuroadrenergic hypertension is produced during 28 da> servo-controlled (SC) intrarenal infusion of decreasing dosages of norepinephrine (NE) in conscious dogs. We examined possible alterations in renal vascular responsiveness during, and subsequent to long-term exposure to SC dosages of intrarenal NE and/or increased arterial pressure. Uninephrectomized, mongrel dogs (n=6, 15.9 +, i.4 kg) were instrumented for chronic study with an arterial catheter, a renal arterial ultrasonic doppler flowprobe and an indwelling nonocclusive renal artery catheter. In vivo steady-state changes in renal vascular resistances (RVR) were determined to angiotensin II (Angll), melhoxamine (MXA), and sodium nitroprusside (NP). In addition, the in vitro renal vascular isometric tension responses to the same vasoactive agonists were compared in control and chronic NE infused kidneys for each dog. In vivo, renal constrictor responses progressively increased over 28 days of intrarenal NE infusion, with an increased response to both Angll (56.6%) and MXA (56.1%) following 28 days of NE infusion compared to control. The renal dilator response to intrarenal NP decreased over 28 days of intrarenal NE înfusion(-13.8%) .In vitro, contractile responses to NE were increased and dilator responses to NP were reduced after 28 days of SC NE infusion. We conclude that long-term, low-level elevations in intrarenal NE and/or increased arterial pressure chronically increase renal vascular adrenergic reactivity combined with reduced vasodilator capacity, fhese vascular changes may contribute to sustained hypertension during chronic low-level elevation of intrarenal NE.