scholarly journals Interaction of the renin-angiotensin system and the renal nerves in the regulation of rat kidney function.

1985 ◽  
Vol 369 (1) ◽  
pp. 311-321 ◽  
Author(s):  
R K Handa ◽  
E J Johns
Keyword(s):  
Kidney Function ◽  
Rat Kidney ◽  
Renin Angiotensin System ◽  
Renal Nerves ◽  
Angiotensin System ◽  
Renin Angiotensin

Renovascular resistance and noradrenaline

1975 ◽  
Vol 229 (6) ◽  
pp. 1649-1653 ◽  
Author(s):  
L Bomzon ◽  
C Rosendorff
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Blocking Agent ◽  
Competitive Inhibitor ◽  
Renal Nerves ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alpha Adrenergic Receptors ◽  
High Doses ◽  
Adrenergic Blocking

Stimulation of the renal nerves can cause cortical vasoconstriction either by direct activation of vascular smooth muscle or by the generation of angiotensin II following renin release from the juxtaglomerular cells. High doses ( greater than 5 mug/min) of the renal neurotransmitter noradrenaline (NA) infused into the renal artery of the baboon causes cortical vasoconstriction. This NA-induced vasoconstriction is significantly reduced (P less than 0.001) by SQ20881, an inhibitor of converting enzyme, and by saralasin, a competitive inhibitor of angiotensin II. These results suggest that NA stimulates the renin-angiotensin mechanism. The further addition of the alpha-adrenergic blocking agent, phenoxybenzamine, to the NA-SQ20881 or NA-saralasin infusate completely abolishes NA-induced cortical vasoconstriction. These results suggest that NA-induced cortical vasoconstriction in the kidney is mediated by activation of both the renin-angiotensin system and alpha-adrenergic receptors.

scholarly journals Comparative efficacy of different renin angiotensin system blockade therapies in patients with IgA nephropathy: a Bayesian network meta-analysis of 17 RCTs

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11661
Author(s):  
Zhihao Huo ◽  
Huizhen Ye ◽  
Peiyi Ye ◽  
Guanqing Xiao ◽  
Zhe Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Network Analysis ◽  
Bayesian Network ◽  
Iga Nephropathy ◽  
Kidney Function ◽  
Meta Analysis ◽  
Renin Angiotensin System ◽  
Cochrane Library ◽  
Angiotensin System ◽  
Renin Angiotensin

Background IgA nephropathy (IgAN) is still one of the most prevalent forms of primary glomerulonephritis globally. However, no guidelines have clearly indicated which kinds of renin angiotensin system blockade therapies (ACEIs or ARBs or their combination) in patients with IgAN result in a greater reduction in proteinuria and a better preservation of kidney function. Thus, we conducted a Bayesian network analysis to evaluate the relative effects of these three therapy regimens in patients with IgAN. Methods The protocol was registered in PROSPERO with ID CRD42017073726. We comprehensively searched the PubMed, the Cochrane Library, Embase, China Biology Medicine disc, WanFang and CNKI databases for studies published since 1993 as well as some grey literature according to PICOS strategies. Pairwise meta-analysis and Bayesian network analysis were conducted to evaluate the effect of different regimens. Results Seventeen randomized controlled trials (RCTs) involving 1,006 patients were analyzed. Co-administration of ACEIs and ARBs had the highest probability (92%) of being the most effective therapy for reducing proteinuria and blood pressure, but ACEIs would be the most appropriate choice for protecting kidney function in IgAN. Conclusion The combination of ACEIs and ARBs seems to have a significantly better antiproteinuric effect and a greater reduction of blood pressure than ACEI or ARB monotherapy in IgAN. ACEIs appear to be a more renoprotective therapy regimen among three therapies.

scholarly journals Renal interactions of renin-angiotensin system, nitric oxide and superoxide anion: implications in the pathophysiology of salt-sensitivity and hypertension

2009 ◽  
pp. S55-S68
Author(s):  
L Kopkan ◽  
L Červenka
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Kidney Function ◽  
Superoxide Anion ◽  
Renin Angiotensin System ◽  
Salt Sensitivity ◽  
Regulatory Function ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Enhanced Production

Renin-angiotensin system (RAS) plays a key role in the regulation of renal function, volume of extracellular fluid and blood pressure. The activation of RAS also induces oxidative stress, particularly superoxide anion (O(2)(-)) formation. Although the involvement of O(2)(-) production in the pathology of many diseases is known for long, recent studies also strongly suggest its physiological regulatory function of many organs including the kidney. However, a marked accumulation of O(2)(-) in the kidney alters normal regulation of renal function and thus may contribute to the development of salt-sensitivity and hypertension. In the kidney, O(2)(-) acts as vasoconstrictor and enhances tubular sodium reabsorption. Nitric oxide (NO), another important radical that exhibits opposite effects than O(2)(-), is also involved in the regulation of kidney function. O(2)(-) rapidly interacts with NO and thus, when O(2)(-) production increases, it diminishes the bioavailability of NO leading to the impairment of organ function. As the activation of RAS, particularly the enhanced production of angiotensin II, can induce both O(2)(-) and NO generation, it has been suggested that physiological interactions of RAS, NO and O(2)(-) provide a coordinated regulation of kidney function. The imbalance of these interactions is critically linked to the pathophysiology of salt-sensitivity and hypertension.

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