The effects of percutaneous transluminal renal angioplasty (PTRA) on the renal function of stenotic kidneys are usually assessed by evaluating the changes in serum creatinine, which is quite a rough indicator of glomerular filtration rate (GFR). In 27 hypertensive patients with 19 atherosclerotic and 11 fibromuscular significant renal artery stenoses, we investigated with renal scintigraphy the short-term (5 days) and long-term (10 months) effects of a technically successful PTRA (in seven cases combined with a stent implantation) on GFR of the stenotic and contralateral kidneys; these measurements were combined with those of plasma renin activity (PRA) and of angiotensin II (AII). We found that in short-term studies after PTRA GFR rose from 29.7 +/- 3.5 to 34.6 +/- 3.1 mL/min and from 36.9 +/- 4.0 to 45.1 +/- 4.3 mL/min, respectively, in atherosclerotic and fibromuscular poststenotic kidneys. In long-term studies GFR further and significantly increased, to 37.8 +/- 3.2 mL/min in the former group, whereas it stabilized in the latter group (46.0 +/- 3.6 mL/min). In patients with fibromuscular stenosis these changes in GFR were associated with clear-cut reductions in blood pressure (BP), PRA, and AII; these decrements also occurred in patients with atherosclerotic stenosis but to a much lesser extent. We also found that in short- and long-term studies the percent of PTRA-induced increments of GFR in the poststenotic kidneys were inversely correlated with the baseline values of GFR. In addition, the absolute and percent increments of GFR were positively correlated with the basal levels of AII. Thus the time course of the improvement in GFR after angioplasty may differ in kidneys, depending on the etiology of the stenosis, in that in those with fibromuscular stenosis it was entirely apparent within a few days whereas in those with atherosclerotic stenosis it required several months to be fully expressed. Also, it appears that the more compromised kidneys are those that benefit most from the dilatation and that AII levels are useful indicators of the possibility that the stenotic kidney will have a favorable functional outcome in terms of restoration of renal blood flow.

No abstract

Selective A2A adenosine receptor agonists are potent vasodilators that reduce blood pressure and induce marked increments in heart rate and plasma renin activity (PRA). To examine the mechanisms and pressor relevance of these cardiac and renin responses, we measured blood pressure and heart rate by telemetry and PRA in separate sets of spontaneously hypertensive rats (SHRs), which were given i.p. 2-hexynyl-5-methylcarboxamidoadenosine (2HE-NECA, 0.01 mg/kg) and 2-[4-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosin e (CGS 21680, 0.1 mg/kg) alone and after pretreatment with the beta 1-adrenoceptor blocking agent atenolol (100 mg/kg). The effects of 2HE-NECA (0.003 mg/kg) also were examined after pretreatment with the angiotensin-converting enzyme (ACE) inhibitor spirapril (3 mg/kg). Both A2A agonists induced marked reductions in blood pressure, associated with significant increments in heart rate and in PRA. Atenolol reduced blood pressure to the same extent as did the A2A agonists and markedly decreased heart rate and PRA. Pretreatment with atenolol entirely prevented the increase in heart rate and in PRA induced by the two A2A agonists but potentiated only slightly their antihypertensive effect. Spirapril alone reduced blood pressure and increased PRA and when given before 2HE-NECA potentiated its depressor and renin-stimulating effects by 44% and 69%, respectively. These results suggest that the increase in heart rate and in PRA induced by A2A agonists is the result of a reflex increase in sympathetic activity triggered by the decrease in blood pressure rather than of a direct stimulating effect on cardiac and renal A2A-adenosine receptors; the reactive activation of the renin-angiotensin system elicited by these compounds may contribute to blunting their antihypertensive effect.

This study was aimed at examining whether four intrarenal echo-Doppler velocimetric indices (pulsatility and resistive indices, acceleration and acceleration time) can be useful for assessing the effects of renal artery dilation obtained with either angioplasty or stent implantation. Echo-Doppler studies were performed in 63 hypertensive patients with 68 renal artery stenoses (39 atherosclerotic and 29 fibromuscular) prior to and within five days after the dilation procedures (55 angioplasties, 13 stent implantations), which resulted in an average reduction of arterial narrowing from 79% to 20%. In 24 patients, the velocimetric indices were also examined in relationship to the venoarterial differences of plasma renin activity and of angiotensin II across the stenotic kidneys. We found that after dilation the values of the four indices had returned within the normal range in all but three arteries (one false negative for resistive index and two for acceleration time). However, decrements in acceleration time was the only factor to be significantly correlated with the reduction of arterial narrowing. Moreover, postdilation values of this index were, on average, slightly but significantly higher in arteries that at follow-up developed restenosis rather than in those that remained patent. For similar reductions in arterial narrowing the absolute changes of all indices were similar in atherosclerotic and fibromuscular stenotic arteries and, in a subset of the atheromatous arteries, were also similar after angioplasty and stent implantation. No relationship was found with the changes in the venoarterial differences of plasma renin activity and angiotensin II. It appears that these intrarenal velocimetric indices and, in particular, acceleration time reliably reflect the technical success of renal artery dilation. The acceleration time index may also be valuable for predicting the restenosis of the dilated vessel. None of the indices, however, mirrors the functional consequences of removal of renal artery stenosis as expressed through the changes in transrenal gradients of the components of the renin-angiotensin system.