Merrill D C, Cowley A W
Am J Physiol. 1986 Mar;250(3 Pt 2):F460-9. doi: 10.1152/ajprenal.1986.250.3.F460.
The effects of chronic (4 days) arginine vasopressin (AVP) infusion were studied in two separate groups of animals: normal Na-restricted dogs with intact renal nerves (n = 8) and renal-denervated Na-restricted dogs (n = 5). Volume expansion during AVP infusion was prevented in these studies with a sensitive servo-controlled cage-scale system. With intravenous AVP infusion (0.36 ng X kg-1 X min-1), plasma AVP levels increased from nearly 3 to 15 pg/ml, whereas total body weight remained unchanged from the control level. In renal-innervated dogs, plasma renin activity (PRA) decreased significantly (P less than 0.05) from control levels of 5.50 +/- 0.61 to an average level of 3.45 +/- 0.76 ng angiotensin I (ANG I) X ml-1 X h-1 on days 1 and 2 of AVP infusion. Thereafter, PRA tended to remain decreased on days 3 and 4, averaging 3.82 +/- 1.02 ng ANG I X ml-1 X h-1, but this was not statistically significant. Urinary Na excretion and balance, however, were not significantly altered during the 4-day AVP infusion period. In renal-denervated dogs, the rise of PRA with Na restriction was 50% that seen in normal dogs. In this group, a transient suppression of PRA was observed on day 1 of AVP infusion from 2.84 +/- 0.75 to 1.46 +/- 0.47 ng ANG I X ml-1 X h-1. Urinary Na excretion increased transiently with a small net Na loss of 4.9 +/- 1.3 meq on day 2 of AVP infusion. No significant changes occurred in average 24-h mean arterial pressure (MAP) in response to AVP in either group of dogs. Thus, in contrast to our previous observations in Na-replete dogs, elevations of plasma AVP within the physiological range result in suppression of PRA, but for periods of no longer than 1-2 days in Na-restricted dogs. This decrease of PRA occurred in the absence of measurable changes in MAP, total body weight, or plasma catecholamines. In addition, this transient AVP-induced suppression of PRA was only partially blunted by prior renal denervation. Finally, in the Na-restricted dog, AVP appears to have minimal or no long-term effects on urinary Na excretion.
在两组不同的动物中研究了慢性(4天)精氨酸加压素(AVP)输注的作用:肾神经完整的正常限钠犬(n = 8)和肾去神经支配的限钠犬(n = 5)。在这些研究中,使用灵敏的伺服控制笼秤系统防止AVP输注期间的容量扩张。静脉输注AVP(0.36 ng·kg⁻¹·min⁻¹)时,血浆AVP水平从近3 pg/ml升高至15 pg/ml,而总体重与对照水平相比保持不变。在肾神经支配的犬中,血浆肾素活性(PRA)在AVP输注的第1天和第2天从对照水平5.50±0.61显著降低(P<0.05)至平均水平3.45±0.76 ng血管紧张素I(ANG I)·ml⁻¹·h⁻¹。此后,PRA在第3天和第4天趋于保持降低,平均为3.82±1.02 ng ANG I·ml⁻¹·h⁻¹,但这无统计学意义。然而,在4天的AVP输注期间,尿钠排泄和平衡没有显著改变。在肾去神经支配的犬中,限钠时PRA的升高是正常犬的50%。在该组中,AVP输注第1天观察到PRA短暂抑制,从2.84±0.75降至1.46±0.47 ng ANG I·ml⁻¹·h⁻¹。AVP输注第2天尿钠排泄短暂增加,有4.9±1.3 meq的少量净钠丢失。两组犬对AVP反应的平均24小时平均动脉压(MAP)均无显著变化。因此,与我们之前在钠充足犬中的观察结果相反,生理范围内血浆AVP升高导致PRA抑制,但在限钠犬中持续时间不超过1 - 2天。PRA的这种降低发生在MAP、总体重或血浆儿茶酚胺无明显可测变化的情况下。此外,这种AVP诱导的PRA短暂抑制仅部分被预先的肾去神经支配减弱。最后,在限钠犬中,AVP似乎对尿钠排泄的长期影响最小或没有影响。