Protein kinase Cβ mediates downregulated expression of glucagon-like peptide-1 receptor in hypertensive rat renal arteries

Liu, Limei; Liu, Jian; Gao, Yuansheng; Ng, Chi Fai; Yu, Xiaoxing; Dou, Dou; Huang, Yü

doi:10.1097/hjh.0000000000000480

Cited by 12 publications

(18 citation statements)

References 39 publications

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“…() and Liu et al. () who also showed that inhibition of protein kinase C (PKC) restored the GLP‐1 induced vasodilation and the expression of the GLP‐1 receptor in renal vessels from SHR. These observations suggest that renal effects of GLP‐1 in SHR are mainly mediated via mechanisms secondary to nonrenal GLP‐1 receptor activation.…”

Section: Discussionmentioning

confidence: 97%

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Glucagon‐like peptide‐1 acutely affects renal blood flow and urinary flow rate in spontaneously hypertensive rats despite significantly reduced renal expression of GLP‐1 receptors

et al. 2017

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Glucagon‐like peptide‐1 (GLP‐1) is an incretin hormone increasing postprandial insulin release. GLP‐1 also induces diuresis and natriuresis in humans and rodents. The GLP‐1 receptor is extensively expressed in the renal vascular tree in normotensive rats where acute GLP‐1 treatment leads to increased mean arterial pressure (MAP) and increased renal blood flow (RBF). In hypertensive animal models, GLP‐1 has been reported both to increase and decrease MAP. The aim of this study was to examine expression of renal GLP‐1 receptors in spontaneously hypertensive rats (SHR) and to assess the effect of acute intrarenal infusion of GLP‐1. We hypothesized that GLP‐1 would increase diuresis and natriuresis and reduce MAP in SHR. Immunohistochemical staining and in situ hybridization for the GLP‐1 receptor were used to localize GLP‐1 receptors in the kidney. Sevoflurane‐anesthetized normotensive Sprague–Dawley rats and SHR received a 20 min intrarenal infusion of GLP‐1 and changes in MAP, RBF, heart rate, dieresis, and natriuresis were measured. The vasodilatory effect of GLP‐1 was assessed in isolated interlobar arteries from normo‐ and hypertensive rats. We found no expression of GLP‐1 receptors in the kidney from SHR. However, acute intrarenal infusion of GLP‐1 increased MAP, RBF, dieresis, and natriuresis without affecting heart rate in both rat strains. These results suggest that the acute renal effects of GLP‐1 in SHR are caused either by extrarenal GLP‐1 receptors activating other mechanisms (e.g., insulin) to induce the renal changes observed or possibly by an alternative renal GLP‐1 receptor.

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Section: Discussionmentioning

confidence: 97%

“…Liu et al. () reported a reduced expression of GLP‐1 receptors in renal arteries from SHR compared to WKY and also in human renal arteries from hypertensive patients based on immunostainings. Quantification based on immunostaining can, however, be extremely difficult.…”

Section: Discussionmentioning

confidence: 99%

Glucagon‐like peptide‐1 acutely affects renal blood flow and urinary flow rate in spontaneously hypertensive rats despite significantly reduced renal expression of GLP‐1 receptors

et al. 2017

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“…Increased expression and activity of PKCs has been shown to enhance VSM contraction and may be involved in hypertension (Sasajima et al , ; Novokhatska et al , ; Liu et al , ; Zhao et al , ). Data of the present study indicate that the increased expression of PKCβ2 in SHR VSM is involved in the exaggerated haemodynamic response to the vascular action of propofol.…”

Section: Discussionmentioning

confidence: 99%

Propofol induces excessive vasodilation of aortic rings by inhibiting protein kinase Cβ2 and θ in spontaneously hypertensive rats

Wang

Zhou

et al. 2017

British J Pharmacology

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“…, Liu et al . ). In mice, GLP‐1R is expressed in the enterocytes lining the villi of jejunum, ileum and colon (jejunum>ileum>colon), paneth cells, mesenteric and submucosal plexus and chromogranin A+ enteroendocrine cells but not in duodenum or the GLP‐1‐secreting L‐cells (Kedees et al .…”

Section: Glp‐1 Receptor Expressionmentioning

confidence: 97%

Mechanisms for the cardiovascular effects of glucagon-like peptide-1

Poudyal

2015

Acta Physiol

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Over the past three decades, at least 10 hormones secreted by the enteroendocrine cells have been discovered, which directly affect the cardiovascular system through their innate receptors expressed in the heart and blood vessels or through a neural mechanism. Glucagon-like peptide-1 (GLP-1), an important incretin, is perhaps best studied of these gut-derived hormones with important cardiovascular effects. In this review, I have discussed the mechanism of GLP-1 release from the enteroendocrine L-cells and its physiological effects on the cardiovascular system. Current evidence suggests that GLP-1 has positive inotropic and chronotropic effects on the heart and may be important in preserving left ventricular structure and function by direct and indirect mechanisms. The direct effects of GLP-1 in the heart may be mediated through GLP-1R expressed in atria as well as arteries and arterioles in the left ventricle and mainly involve in the activation of multiple pro-survival kinases and enhanced energy utilization. There is also good evidence to support the involvement of a second, yet to be identified, GLP-1 receptor. Further, GLP-1(9-36)amide, which was previously thought to be the inactive metabolite of the active GLP-1(7-36)amide, may also have direct cardioprotective effects. GLP-1's action on GLP-1R expressed in the central nervous system, kidney, vasculature and the pancreas may indirectly contribute to its cardioprotective effects.

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Protein kinase Cβ mediates downregulated expression of glucagon-like peptide-1 receptor in hypertensive rat renal arteries

Abstract: The present results provide novel evidence that the reduced GLP-1R expression in SHR renal arteries is most likely mediated through PKCβ upregulation; the latter probably contributes to the impaired GLP-1R-mediated vasorelaxations in hypertension.

Cited by 12 publications

References 39 publications

Glucagon‐like peptide‐1 acutely affects renal blood flow and urinary flow rate in spontaneously hypertensive rats despite significantly reduced renal expression of GLP‐1 receptors

Glucagon‐like peptide‐1 acutely affects renal blood flow and urinary flow rate in spontaneously hypertensive rats despite significantly reduced renal expression of GLP‐1 receptors

Propofol induces excessive vasodilation of aortic rings by inhibiting protein kinase Cβ2 and θ in spontaneously hypertensive rats

Mechanisms for the cardiovascular effects of glucagon-like peptide-1

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