Renal vascular resistance

Together with the increase in cardiac output, renal blood flow is also increased with a significant decrease in renal vascular resistance(10). 

In the same study, neither the renal blood flow nor the renal vascular resistances were found to be affected by P840 (data not shown). 

Pharmacology Initially, clonidine stimulates peripheral -adrenergic receptors producing transient vasoconstriction. Stimulation of alpha-adrenergic in the brain stem results in reduced sympathetic outflow from the CNS and a decrease in peripheral resistance, renal vascular resistance, heart rate, and blood pressure. Pharmacokinetics Blood pressure declines within 30 to 60 minutes after an oral... 

Reduction in arterial blood pressure by clonidine is accompanied by decreased renal vascular resistance and maintenance of renal blood flow. As with methyldopa, clonidine reduces blood pressure in the supine position and only rarely causes postural hypotension. Pressor effects of clonidine are not observed after ingestion of therapeutic doses of clonidine, but severe hypertension can complicate a massive overdose. 

Depending on the concentration, volatile anesthetics decrease the glomerular filtration rate and renal blood flow, and increase the filtration fraction. Since renal blood flow decreases during general anesthesia in spite of well-maintained or even increased perfusion pressures (due to increased renal vascular resistance), autoregulation of renal flow may be impaired by these drugs. 

Most cardiovascular reflexes remain intact after administration of methyldopa, and blood pressure reduction is not markedly dependent on maintenance of upright posture. Postural (orthostatic) hypotension sometimes occurs, particularly in volume-depleted patients. One potential advantage of methyldopa is that it causes reduction in renal vascular resistance. 

The loop diuretics act promptly, even in patients who have poor renal function or who have not responded to thiazides or other diuretics. The loop diuretics cause decreased renal vascular resistance and increased renal blood flow. [Note Loop diuretics increase the Ca++ content of urine (see p. 227), whereas thiazide diuretics decrease the Ca++ concentration of the urine.]... 

Renal function is limited at birth because the kidneys are anatomically and functionally immature. In full-term newborns, glomerular filtration rate (GFR) is 10-15 mL/min/m, and in premature infants the GFR is only 5-10 mL/min/m. GFR doubles by 1 week of age, because of a postnatal drop in renal vascular resistance and increase in renal blood flow, and reaches adult values by 1 year of age (Figure 23.6) (40,41). A glomerular/tubular imbalance is present in newborns, because glomerular function matures more... 

Similarly, renal function is markedly affected by the renovascular actions of endothelin [47]. However, the presence of non-vascular endothelin receptor sites in the kidney suggests that endothelin may modulate renal function by a direct action [48]. Indeed, a direct contractile and mitogenic action of ET-1 on mesangial cells has been demonstrated [49]. The different isoforms show different profiles in the kidney. ET-1 increases renal vascular resistance and glomerular filtration rate [50]. ET-3, however, decreases renal flow and GFR at low doses, although higher doses produce effects similar to those seen with ET-1 [51]. 

Ornipressin is a vasopressin analogue that primarily leads to vasoconstriction of the splanchnic vasculature. The first report outlining its use was compiled in 1985 by K. Lenz et al. (36) Dosage was 25 IU/12 hr or 6 IU/4 hr. The outcome was a fall in renal vascular resistance and an improvement in the glomerular filtration rate. (23 quot. 6, 10, 12, 43) The combined administration of ornipressin (2-6 lU/hr) and albumin (20-60 g/day) for a period of 2 weeks (with intensive care monitoring ) has led to remarkable therapeutic success. (24)... 

The IPRK was used to demonstrate that excess nitric oxide (NO) and possibly endothelium-derived hyperpolarizing factor (EDHF), contribute to impaired autoregulation after ischemic injury as described above [328]. A role for EDHF in renal vascular resistance and in glomerular and tubular function was first observed in the IPRK by Bhardwaj and Moore [386] and by Rademacher et al [387-8]. Others observed that manipulating NO can alter medullary oxygenation in the IPRK [288]. An increased endothelium-dependent vasodilator response to acetylcholine was observed in IPRK from cirrhotic rats [390]. Portal vein ligation also... 

Ratcliffe PJ, Endre ZH, Nicholls LG,Tange JD, Ledingham JGG The isolated perfused rat kidney filtering and non-filtering models in the assessment of altered renal vascular resistance in nephrotoxicity, in Nephrotoxicity Extrapolation from in vitro to in vivo and from animalsto man., edited by Bach PH, Lock EA, New York, Plenum, 1989, pp 107-110... 

Radermacher J, Forstermann U, Frolich JC Endothelium-derived relaxing factor influences renal vascular resistance. Am J Physiol 259 9-17,1990... 

Infusions of AmB, intravenously or into the renal artery, induce short-term reduction in renal blood flow (RBF) and GFR, and an increase in renal vascular resistance, in both rats and dogs [83-85]. The effects of short term infusions of AmB on the renal microcirculation in rats revealed that the single nephron GFR was decreased by 2 mechanisms (Table 1) 1) a decrease in single nephron plasma flow, due to vasoconstriction of the afferent and efferent arterioles, and 2) a reduction in the glomerular capillary ultrafiltration coefficient (Kf), an effect probably mediated by mesangial cell contraction [86]. Previous micropuncture studies demonstrated a similar vasoconstriction of the afferent arteriole but also an increased permeability of the tubular epithelium to inulin [75]. Thus, the reduction in GFR after acute AmB infusions can be attributed to contraction of afferent smooth muscle cells, efferent smooth muscle cells and glomerular mesangial cells, as well as increased tubular permeability with back-leak... 

In most studies in which it has been investigated, ethacrynic acid administration results in a marked reduction in renal vascular resistance [13, 19-21]. However, this effect is nullified, as in the case with furosemide, by the superimposition of volume depletion [20-22]- Studies of bumetanide in the experimental animal have generally shown no change in GFR or renal plasma flow (RPF) [23, 24] except for transient acute increases in the latter which approximated 27 to 40%, declining later in the experiments to only modest elevations or to control levels [25,26]. In man, bumetanide is associated with either no change [27,28] or a 12 to 16% increase in effective renal plasma flow and glomerular filtration rate [29]. 

Tacrolimus causes acute reversible renal dysfunction in renal [661-663,667], hver [290,664-666,679,680], heart [681-683] and pulmonary [684, 685] transplant recipients and in patients with immunologically mediated diseases [686]. Tacrolimus-induced GFR and RBF decrease is associated with an important increase in renal vascular resistance, both in humans and rodents [63,679,687-692]. Calcium channel blockers improved renal function in TAC-treated liver transplant recipients [693] and in animal models of TAC nephrotoxicity [689,694-6%]. Tacrohmus acute nephrotoxicity, similar to CSA, shows normal renal histology or non-specific changes such as isometric cytoplasmic vacuolation in tubular epithelial cells, microcalcification, giant mitochondria and lysosomes, and necrosis and early hyahnosis of individual smooth muscle cells in the afferent arterioles, which revert with drug reduction or discontinuation [697-699]. 

Clinical and animal studies suggest that TAC and CSA may have distinct effects on renal vascular resist-... 

BenignI A, Morigl M, Perico N, Zoja C, Amuchastegul CS, PIccinelll A, Donadelll R, RemuzzI G. The acute effect of EK506 and cyclosporine on endothelial cell function and renal vascular resistance. Transplantation 1992 54 775-780. 

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