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Fulltext Interaction between nitric oxide and renal α1-adrenoreceptors mediated vasoconstriction in rats with left ventricular hypertrophyin Wistar Kyoto rats

Ahmad A, Sattar MA, Azam M, Khan SA, Bhatt O, Johns EJ

PLoS One, 2018;13(2):e0189386.
PMID: 29447158 DOI: 10.1371/journal.pone.0189386

Left ventricular hypertrophy (LVH) is associated with decreased responsiveness of renal α1-adrenoreceptors subtypes to adrenergic agonists. Nitric oxide donors are known to have antihypertrophic effects however their impact on responsiveness of renal α1-adrenoreceptors subtypes is unknown. This study investigated the impact of nitric oxide (NO) and its potential interaction with the responsiveness of renal α1-adrenoreceptors subtypes to adrenergic stimulation in rats with left ventricular hypertrophy (LVH). This study also explored the impact of NO donor on CSE expression in normal and LVH kidney. LVH was induced using isoprenaline and caffeine in drinking water for 2 weeks while NO donor (L-arginine, 1.25g/Lin drinking water) was given for 5 weeks. Intrarenal noradrenaline, phenylephrine and methoxamine responses were determined in the absence and presence of selective α1-adrenoceptor antagonists, 5- methylurapidil (5-MeU), chloroethylclonidine (CeC) and BMY 7378. Renal cortical endothelial nitric oxide synthase mRNA was upregulated 7 fold while that of cystathione γ lyase was unaltered in the NO treated LVH rats (LVH-NO) group compared to LVH group. The responsiveness of renal α1A, α1B and α1D-adrenoceptors in the low dose and high dose phases of 5-MeU, CEC and BMY7378 to adrenergic agonists was increased along with cGMP in the kidney of LVH-NO group. These findings suggest that exogenous NO precursor up-regulated the renal eNOS/NO/cGMP pathway in LVH rats and resulted in augmented α1A, α1B and α1D adrenoreceptors responsiveness to the adrenergic agonists. There is a positive interaction between H2S and NO production in normal animals but this interaction appears absent in LVH animals.

Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology*
Left ventricular hypertrophy and its relation to the cardiac kinin-forming system in hypertensive and diabetic rats

Sharma JN, Uma K, Yusof AP

Int J Cardiol, 1998 Feb 28;63(3):229-35.
PMID: 9578349 DOI: 10.1016/s0167-5273(97)00329-x

We investigated the cardiac tissue kallikrein and kininogen levels, left ventricular wall thickness and mean arterial blood pressure of Wistar Kyoto and spontaneously hypertensive rats with and without streptozotocin-induced diabetes. The mean arterial blood pressure was highly elevated (P<0.001) in Wistar Kyoto diabetic and spontaneously hypertensive diabetic rats as compared with their respective controls. The cardiac tissue kallikrein and kininogen levels were reduced significantly (P<0.001) in diabetic Wistar Kyoto, spontaneously hypertensive and diabetic spontaneously hypertensive compared with Wistar Kyoto control rats. In addition, the left ventricular thickness was found to be increased (P<0.001) in diabetic Wistar Kyoto and spontaneously hypertensive rats in the presence and in the absence of diabetes. Our results indicate that reduced activity of the kinin-forming system may be responsible for inducing left ventricular hypertrophy in the presence of raised mean arterial blood pressure in diabetic and hypertensive rats. Thus, the kinin-forming components might have a protective role against the development of left ventricular hypertrophy. The possible significance of these findings is discussed.

Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology*
Left ventricular hypertrophy and chronic fluid overload in peritoneal dialysis patients

Cader RA, Ibrahim OA, Paul S, Gafor HA, Mohd R

Int Urol Nephrol, 2014 Jun;46(6):1209-15.
PMID: 24307428 DOI: 10.1007/s11255-013-0615-8

PURPOSE: Cardiovascular disease is the leading cause of mortality in dialysis patients with left ventricular hypertrophy (LVH) being an important predictor of mortality. We wanted to determine the prevalence of LVH in peritoneal dialysis (PD) patients and factors contributing to it.
METHODS: This is a cross-sectional study assessing LVH using echocardiogram in PD patients. Left ventricular mass index (LVMI) was calculated to determine LVH. Chronic fluid overload (overhydration) was assessed using the body composition monitor, and blood pressure (BP) was measured using 24-h ambulatory BP monitoring.
RESULTS: Thirty-one patients (21 females:10 males, 48.97 ± 14.50 years and dialysis vintage 40.0 ± 28.9 months) were studied. More than two-thirds (77.4 %) were hypertensive, and a third (35.5 %) were diabetic. Baseline data included mean serum albumin (37.34 ± 4.43 g/l), weekly Kt/V (2.02 ± 0.23), residual renal function of 68 (0-880) ml and ultrafiltration of 1,606.9 ± 548.6 ml. Majority of patients (80.6 %) had LVH on echocardiogram with LVMI of 136.5 ± 37.8 g/m(2) and overhydration of 2.23 ± 1.77 l. Average systolic BP, diastolic BP and mean arterial pressure were 141.2 ± 23.3, 90.8 ± 19.7 and 107.6 ± 19.6 mmHg, respectively. Patients with LVH had a lower serum albumin (p = 0.003), were more overhydrated (p = 0.010) and were on higher number of anti-hypertensive agents (p ≤ 0.001). Predictors of LVMI were overhydration (p = 0.002), the presence of diabetes (p = 0.008) and the number of anti-hypertensive agents used (p = 0.026). However, overhydration (p = 0.007) was the main predictor of LVH on multivariate analysis.
CONCLUSION: Overhydration is strongly associated with LVH in PD patients.

Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology
Effect of captopril on urinary kallikrein, blood pressure and myocardial hypertrophy in diabetic spontaneously hypertensive rats

Sharma JN, Kesavarao U

Pharmacology, 2002 Apr;64(4):196-200.
PMID: 11893900 DOI: 10.1159/000056171

We investigated the total urinary kallikrein levels, left-ventricular wall thickness and mean arterial blood pressure of nontreated and captopril-treated diabetic and nondiabetic spontaneously hypertensive rats. The mean arterial blood pressure was significantly elevated in diabetic spontaneously hypertensive rats as compared to nondiabetic spontaneously hypertensive rats. Captopril treatment caused a significant reduction in the arterial blood pressure of both nondiabetic and diabetic spontaneously hypertensive rats. The left-ventricular wall thickness was also significantly reduced in diabetic and nondiabetic spontaneously hypertensive treated with captopril as compared to nontreated diabetic and nondiabetic spontaneously hypertensive rats. The total urinary kallikrein levels were significantly raised in captopril-treated diabetic and nondiabetic spontaneously hypertensive rats against the values obtained from nontreated diabetic and nondiabetic spontaneously hypertensive rats. These results indicate that blood pressure reduction and left ventricular wall regression with captopril treatment might be due to enhanced renal kallikrein formation. The significance of these findings is discussed.

Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology*
Ablation of IL-33 gene exacerbate myocardial remodeling in mice with heart failure induced by mechanical stress

Veeraveedu PT, Sanada S, Okuda K, Fu HY, Matsuzaki T, Araki R, et al.

Biochem Pharmacol, 2017 Aug 15;138:73-80.
PMID: 28450225 DOI: 10.1016/j.bcp.2017.04.022

BACKGROUND AND PURPOSE: ST2 is one of the interleukin (IL)-1 receptor family members comprising of membrane-bound (ST2L) and soluble (sST2) isoforms. Clinical trials have revealed that serum sST2 levels predict outcome in patient with myocardial infarction or chronic heart failure (HF). Meanwhile, we and others have reported that ablation of ST2 caused exaggerated cardiac remodeling in both ischemic and non-ischemic HF. Here, we tested whether IL-33, the ligand for ST2, protects myocardium against HF induced by mechanical overload using ligand specific knockout (IL-33(-/-)) mice.
METHODS AND RESULTS: Transverse aortic constriction (TAC)/sham surgery were carried out in both IL-33 and WT-littermates. Echocardiographic measurements were performed at frequent interval during the study period. Heart was harvested for RNA and histological measurements. Following mechanical overload by TAC, myocardial mRNA expressions of Th1 cytokines, such as TNF-α were enhanced in IL-33(-/-) mice than in WT mice. After 8-weeks, IL-33(-/-) mice exhibited exacerbated left ventricular hypertrophy, increased chamber dilation, reduced fractional shortening, aggravated fibrosis, inflammation, and impaired survival compared with WT littermates. Accordingly, myocardial mRNA expressions of hypertrophic (c-Myc/BNP) molecular markers were also significantly enhanced in IL-33(-/-) mice than those in WT mice.
CONCLUSIONS: We report for the first time that ablation of IL-33 directly and significantly leads to exacerbate cardiac remodeling with impaired cardiac function and survival upon mechanical stress. These data highlight the cardioprotective role of IL-33/ST2 system in the stressed myocardium and reveal a potential therapeutic role for IL-33 in non-ischemic HF.

Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology
Functional contribution of α1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar-Kyoto rats

Ahmad A, Sattar MA, Rathore HA, Abdulla MH, Khan SA, Abdullah NA, et al.

Can J Physiol Pharmacol, 2014 Dec;92(12):1029-35.
PMID: 25403946 DOI: 10.1139/cjpp-2014-0236

This study investigated the role of α1D-adrenoceptor in the modulation of renal haemodynamics in rats with left ventricular hypertrophy (LVH). LVH was established in Wistar-Kyoto (WKY) rats with isoprenaline (5.0 mg · (kg body mass)(-1), by subcutaneous injection every 72 h) and caffeine (62 mg · L(-1) in drinking water, daily for 14 days). Renal vasoconstrictor responses were measured for noradrenaline (NA), phenylephrine (PE), and methoxamine (ME) before and immediately after low or high dose intrarenal infusions of BMY 7378, a selective α1D-adrenoceptor blocker. The rats with LVH had higher mean arterial blood pressure and circulating NA levels, but lower renal cortical blood perfusion compared with the control group (all P < 0.05). In the LVH group, the magnitude of the renal vasoconstrictor response to ME was blunted, but not the response to NA or PE (P < 0.05), compared with the control group (LVH vs. C, 38% vs. 50%). The magnitude of the drop in the vasoconstrictor responses to NA, PE, and ME in the presence of a higher dose of BMY 7378 was significantly greater in the LVH group compared with the control group (LVH vs. C, 45% vs. 25% for NA, 52% vs. 33% for PE, 66% vs. 53% for ME, all P < 0.05). These findings indicate an impaired renal vasoconstrictor response to adrenergic agonists during LVH. In addition, the α1D-adrenoceptor subtype plays a key role in the modulation of vascular responses in this diseased state.

Matched MeSH terms: Hypertrophy, Left Ventricular/physiopathology