PDF(Pubmed)
Abstract：
Experimental glomerulonephritis results in hypertension that is sensitive to salt. Nevertheless, salt retention alone cannot explain the increase in blood pressure. Angiotensin antagonistic therapy reduces hypertension caused by puromycin amino nucleosides (PAN). We investigated the hypothesis that PAN modifies renal vascular reactivity through processes dependent on angiotensin. Long-Evans rats were given an intraperitoneal injection of either puromycin (150 mg/kg) or saline (controls). Group 1 was fed a normal sodium diet (NSD, n = 9). Group 2 was given 30 mg/L of quinapril (Q) in addition to NSD (NSD + Q; n = 6). Group 3 received a high sodium diet (HSD, n = 7), and Group 4 received HSD + Q (n = 7). Systolic blood pressure (SBP), plasma creatinine, proteinuria, and sodium balance were monitored for 12 days. On day 15, renal vascular reactivity was assessed by administering increasing doses of angiotensin II, acetylcholine (ACh), and sodium nitroprusside (SNP) directly into the renal artery. SBP progressively increased in all PAN groups. This increase in SBP was greater in the HSD groups and was not significantly altered by Q treatment. SBP increased by 22 ± 4% (NSD), 51 ± 5% (NSD + Q), 81 ± 10% (HSD), and 65 ± 8% (HSD + Q). The renal blood flow of PAN rats did not return to baseline despite their normal renal vasoconstrictor responses to angiotensin II. Additionally, they showed reduced renal vasodilator responses to SNP and Ach. The vasodilator responses to both vasodilators were surprisingly unaffected by the inhibition of the angiotensin-converting enzyme (ACE). Renal vasodilator responses to both endothelium-dependent and independent variables were reduced in early PAN-induced hypertension. We found that the angiotensin-mediated mechanism is not responsible for this altered renal vasoreactivity.
摘要：
实验性肾小球肾炎导致对盐敏感的高血压。然而，仅靠盐潴留不能解释血压的升高。血管紧张素拮抗治疗可减少由嘌呤霉素氨基核苷（PAN）引起的高血压。我们调查了PAN通过依赖于血管紧张素的过程来修饰肾血管反应性的假设。Long-Evans大鼠腹膜内注射嘌呤霉素(150mg/kg)或盐水(对照)。第1组饲喂正常钠饮食(NSD，n=9)。除NSD外，第2组还给予30mg/L的喹那普利（Q）（NSDQ；n=6）。第3组接受高钠饮食（HSD，n=7),第4组接受HSD+Q(n=7)。收缩压（SBP），血浆肌酐,蛋白尿,监测钠平衡12天。在第15天，通过增加剂量的血管紧张素II来评估肾血管反应性，乙酰胆碱（ACh），和硝普钠（SNP）直接进入肾动脉。在所有PAN组中SBP逐渐增加。在HSD组中SBP的这种增加更大,并且通过Q处理没有显著改变。SBP增加22±4%（NSD），51±5%(NSD+Q),81±10%(HSD),和65±8%(HSD+Q)。尽管PAN大鼠对血管紧张素II的肾血管收缩反应正常，但其肾血流量仍未恢复至基线。此外,他们显示肾血管扩张剂对SNP和Ach的反应降低.令人惊讶的是，两种血管扩张剂的血管扩张剂反应均不受血管紧张素转换酶（ACE）抑制的影响。在早期PAN诱导的高血压中，肾脏对内皮依赖性和自变量的血管舒张反应均降低。我们发现血管紧张素介导的机制与这种改变的肾血管反应性无关。
