Role of angiotensin in ameliorating the renal actions of norepinephrine

Yang, Hye-Won; Lohmeier, Thomas E.

doi:10.1152/ajpregu.1991.261.6.r1497

Cited by 4 publications

(7 citation statements)

References 19 publications

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“…A more or less pronounced decrease in renal function following ACEI administration has been described in dogs with experimental renal artery stenosis (Brooks et al. , 1992), acute renal adrenergic stimulation (Yang & Lohmeier, 1991), or excessive ACEI dosages (MacDonald et al. , 1987).…”

Section: Acute Renal Failurementioning

confidence: 99%

Angiotensin‐converting enzyme inhibitors in the therapy of renal diseases

Lefebvre

Toutain

2004

Vet Pharm & Therapeutics

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Renal diseases, especially chronic renal failure (CRF), are common in canine and feline medicine. The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in these conditions in the development of renal lesions and the progression of kidney dysfunction. Angiotensin-converting enzyme inhibitors (ACEI) are currently considered as the most efficient agents in therapeutic strategies. The benefit of an ACEI treatment can be explained by at least three mechanisms: ACEI limit systemic and glomerular capillary hypertension, have an antiproteinuric effect, and retard the development of glomerulosclerosis and tubulointerstitial lesions. These effects have been studied in dogs and cats, and there is now some evidence to support the recommendation of ACEI therapy in dogs and cats with CRF. Nevertheless the prescription of ACEI in such patients should take into account the potential influence of renal impairment on ACEI disposition, and adverse effects on the renal function itself (especially hypotension and acute reductions in glomerular filtration rate). The risk of drug interaction with diuretics, nonsteroidal anti-inflammatory drugs and anesthetics, should not be overestimated. Furthermore, hypotension may occur in patients on a low sodium diet.

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Section: Acute Renal Failurementioning

confidence: 99%

Angiotensin‐converting enzyme inhibitors in the therapy of renal diseases

Lefebvre

Toutain

2004

Vet Pharm & Therapeutics

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“…3 " 13 In previous studies, acute blockade of the renin-angiotensin system either has attenuated or has had no effect on the RBF response to adrenergic stimulation. In contrast, in two earlier studies from our laboratory we observed that long-term administration of captopril actually increased the sensitivity of the renal vasculature to chronic intrarenal infusions of NE, causing severe renal ischemia at rates of NE infusion that produced only moderate reductions in renal plasma flow in dogs with a functional renin-angiotensin system.…”

Section: Discussionmentioning

confidence: 96%

“…In previous studies, we observed that captopril enhanced the renovascular response to intrarenal infusions of NE that produced 20-40% reductions in renal plasma flow when the renin-angiotensin system was intact. 6 - 13 However, since renal plasma flow was determined only after hours to days of continuous renal adrenergic stimulation, the significance of these findings is unclear because it is uncertain that neurally induced reductions in RBF of this magnitude would be sustained for such long periods of time under either physiological or pathophysiological conditions. The present results, on the other hand, showed that severe renal ischemia may occur very abruptly during moderate increments in renal adrenergic stimulation when the renin-angiotensin system is chronically blocked with captopril.…”

Section: Discussionmentioning

confidence: 99%

“…At the lowest infusion rates of NE used, which decreased RBF 11-33% under control conditions, there was a pronounced reduction in the renal vasoconstriction produced by NE when plasma levels of Ang II were fixed at control levels, relative to the response before captopril administration when Ang II was capable of increasing above control levels ( Figure 1). Because these low rates of NE infusion into the renal artery increase renin release, 13 it is likely that increased generation of Ang II normally contributes to the renal vasoconstriction produced by NE. This is consistent with the findings of Pelayo et al 9 during electrical renal nerve stimulation in rats.…”

Section: Discussionmentioning

confidence: 99%

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Influence of endogenous angiotensin on the renovascular response to norepinephrine.

Yang

Lohmeier

1993

Hypertension

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The purpose of this study was to elucidate the role of endogenous angiotensin II in mediating the renovascular effects of renal adrenergic stimulation. Six conscious dogs instrumented for monitoring of renal blood flow were subjected to step increases every 10 minutes in the rate of norepinephrine infusion into the renal artery. Under control conditions, infusion of norepinephrine (10-40 ng/min per milliliter per minute of control renal blood flow) increased plasma renin activity and decreased renal blood flow progressively by -10-75%. When increments in angiotensin II during norepinephrine infusion were abolished by fixing plasma levels of angiotensin II at either normal or high concentrations by chronic infusion of captopril plus angiotensin II, renal blood flow responses to adrenergic stimulation were greatly attenuated at rates of norepinephrine infusion that decreased renal blood flow up to -40% under control conditions. Thus, acutely generated angiotensin II appeared to contribute to the renovascular effects of norepinephrine. However, when endogenous levels of angiotensin II were suppressed to low levels by chronic infusion of captopril alone, norepinephrine induced severe renal ischemia at much lower rates of infusion than occurred when the renin-angiotensin system was intact. Since this enhanced sensitivity to norepinephrine did not occur during chronic captopril infusion when angiotensin II was given simultaneously at rates that restored mean arterial pressure to normotensive levels or higher, low arterial pressure during chronic captopril administration may predispose the kidneys to excessive renal vasoconstriction during renal adrenergic stimulation. Because both norepinephrine (NE) released from adrenergic nerve terminals and angiotensin II (Ang II) generated in response to renal nerve stimulation have potent direct effects on renal hemodynamics and sodium excretion, blockers of the renin-angiotensin system have been given in a number of studies to determine the contribution of increased Ang II generation to the renal hemodynamic and antinatriuretic effects of renal adrenergic stimulation. The most consistent finding from these studies has been that Ang II, presumably by preferentially constricting the efferent arterioles, plays a significant role in the maintenance of glomerular filtration rate during reductions in renal blood flow (RBF) produced by neural stimulation. 3 " 6 The role of generated Ang II in mediating the RBF and sodium excretory responses produced byTenal adrenergic stimulation, however, has been more controversial.

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“…Tubular lesions, interstitial fibrosis, and interstitial inflammatory cell infiltrate were scored similarly from 0 (normal) to 3 (severe change)(from [50]). dogs [66,67]. Acute renal failure potentially due to ACE inhibitors has been reported in dogs treated with captopril [68], enalapril [68] and benazepril [69].…”

Section: Specific Adverse Effects Of Ace Inhibitors Reported In Dogsmentioning

confidence: 99%

Angiotensin-Converting Enzyme Inhibitors in Veterinary Medicine

Lefebvre¹,

Brown²,

Chetboul³

et al. 2007

CPD

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Angiotensin-converting enzyme (ACE) inhibitors represent one of the most commonly used categories of drugs in canine and feline medicine. ACE inhibitors currently approved for use in veterinary medicine are benazepril, enalapril, imidapril and ramipril. They are all pro-drugs administered by oral route. A physiologically based model taking into account the saturable binding to ACE has been developed for pharmacokinetic analysis. The bioavailability of the active compounds from their respective pro-drug is low. The active metabolites are eliminated by renal, hepatorenal or biliary excretion, according to the drug. The elimination half-life of the free fraction of the active compounds is very short (ranging from approximately 10 min to 2 h). ACE inhibitors are generally well tolerated. Benazepril, enalapril, imidapril and ramipril are approved for dogs with chronic heart failure (CHF). The efficacy of ACE inhibitors has been convincingly demonstrated in dogs with CHF, especially in those with chronic valvular disease. In such clinical settings, ACE inhibitors improve hemodynamics and clinical signs, and increase survival time. In cats with cardiovascular disease, little information is available except for reports of some benefit in cats with hypertrophic cardiomyopathy in two non-controlled investigations. ACE inhibitors have also a mild to moderate hypotensive effect. There is also evidence to recommend ACE inhibitors in dogs and cats with chronic renal failure (CRF). They decrease the glomerular capillary pressure, have antiproteinuric effects, tend to delay the progression of CRF and to limit the extent of renal lesions.

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Role of angiotensin in ameliorating the renal actions of norepinephrine

Cited by 4 publications

References 19 publications

Angiotensin‐converting enzyme inhibitors in the therapy of renal diseases

Angiotensin‐converting enzyme inhibitors in the therapy of renal diseases

Influence of endogenous angiotensin on the renovascular response to norepinephrine.

Angiotensin-Converting Enzyme Inhibitors in Veterinary Medicine

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