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1 GFR coincided with a significant increase in renal vascular resistance.
2 s, which may contribute to autoregulation of renal vascular resistance.
3 .2 to 6.8+/-0.4 ml/min x g) and decreases in renal vascular resistance.
4 d in mediating autoregulatory adjustments in renal vascular resistance.
5 lar filtration rate (21%, p<0.05), decreased renal vascular resistance (18%, p<0.05) but caused no si
6 idence interval of indirect effect including renal vascular resistance, -2.51 to -0.76).
7 fective renal plasma flow and an increase in renal vascular resistance (all P<0.01).
8 cline was associated with an 84% increase in renal vascular resistance and a 54% reduction in GFR (ba
9 ained increase in mean arterial pressure and renal vascular resistance and a decrease in heart rate (
10                      The reduction of BP and renal vascular resistance and associated substantial nat
11 ministration showed no significant effect on renal vascular resistance and blood flow.
12 creases in renal blood flow and decreases in renal vascular resistance and distal tubular sodium reab
13 d vessels and leads to a marked reduction in renal vascular resistance and enhancement of renal blood
14 s, including renal artery pulsatility index, renal vascular resistance, and arterial volume in the co
15 flow (indicator-dilution technique), reduced renal vascular resistance, and produced a slight increas
16 nerve activity in control of blood pressure, renal vascular resistance, and sodium excretion.
17 ; P < 0.01 versus BQ-123), reduced effective renal vascular resistance (BQ-123, -1.2 +/- 3.1%; BQ-123
18 1.8+/-0.2 to 2.8+/-0.2 ml/min) and decreased renal vascular resistance by 42% (from 55+/-7.5 to 31.8+
19 ncreased renal blood flow by 84% and reduced renal vascular resistance by 48%.
20 Hg during the 2 wk in the diabetic rats, and renal vascular resistance decreased.
21 mportant in the control of renin release and renal vascular resistance during salt deprivation.
22  In contrast, ERPF was reduced and effective renal vascular resistance (ERVR) increased in both group
23 l plasma flow (ERPF) and decreases effective renal vascular resistance (ERVR) with no significant cha
24 angiotensin system exerts tonic control over renal vascular resistance in mice to a greater extent th
25                                              Renal vascular resistance index (RVR units) was calculat
26  the later stages of HPP reflects increasing renal vascular resistance localized at a postglomerular
27 oline also caused a significant reduction in renal vascular resistance (maximal reduction 55+/- 6%) a
28 nulin clearance (index of GFR) and increased renal vascular resistance (measured by transit time nano
29 ower arterial volume in the cortex or higher renal vascular resistance, respectively, when offered as
30 ygenation, and function through reduction in renal vascular resistance, reversal of endothelial dysfu
31 . min(-1). g(-1) (P < 0.01) and elevation of renal vascular resistance (RVR) (day 6 versus day 14, 15
32 hesis that autoregulation-related changes in renal vascular resistance (RVR) are mediated by extracel
33                    During the RAP reduction, renal vascular resistance (RVR) decreased and upon rapid
34 RAP was increased, the myogenic component of renal vascular resistance (RVR) rapidly rose within the
35                   Despite a lower MAP, basal renal vascular resistance (RVR) was higher during endoto
36 pler flow wire in the renal artery), RBF and renal vascular resistance (RVR) were evaluated.
37                                         RBF, renal vascular resistance (RVR), GFR, and urine flow did
38 ion preservation (HPPP), oxygen consumption, renal vascular resistance (RVR), pH, pCO2, and perfusion
39 , Delta = -1.8 to 2.9 ml min(-1)), increased renal vascular resistance (RVR, Delta = +47 to 54 mmHg m
40 r or the angiotensin-converting enzyme gene, renal vascular resistance was significantly lower than i
41 to a dose-dependent normalization of RBF and renal vascular resistance within 2 h of cross-clamp remo

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