Vasodilator efficiency of endogenous prostanoids, Ca2+-activated K+ channels and nitric oxide in rats with spontaneous, salt-dependent or NO-deficient hypertension

Behuliak, Michal; Pintérová, M.; Kuneš, Jaroslav; Zicha, Josef

doi:10.1038/hr.2011.82

Cited by 19 publications

(11 citation statements)

References 35 publications

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“…An elevated sympathetic tone in SHR was shown previously [19, 20] and our observation of increased heart rate in SHR at both ages studied is in agreement with these studies. Moreover, it has been reported that the hyperactivity of the sympathetic nervous system could induce structural and functional alterations of the heart and blood vessels in SHR [20, 64–66].…”

Section: Discussionsupporting

confidence: 94%

“…Moreover, it has been reported that the hyperactivity of the sympathetic nervous system could induce structural and functional alterations of the heart and blood vessels in SHR [20, 64–66]. In addition, age-related decrease in the NO-dependent relaxation in the femoral artery along with its structural remodeling may be implicated in the pathogenesis of peripheral artery disease.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, the BP of WKY reaches adult levels by the 10th week of age [19]. High blood pressure in SHR may result from sympathetic hyperactivity and sympathetic vasoconstriction [20, 21]. In SHR, the femoral artery, a conductance medium-size artery, exhibits increased vasoconstriction to the sympathetic vasoconstrictor noradrenaline [22–24] and endothelial dysfunction in adulthood [25].…”

Section: Introductionmentioning

confidence: 99%

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Age-Related Alterations in Endothelial Function of Femoral Artery in Young SHR and WKY Rats

Púzserová

Ilovska

Bališ

et al. 2014

BioMed Research International

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The present study was designed to evaluate the effects of vascular aging in juvenescence on endothelial function in femoral arteries and to assess differences between normotensive and hypertensive rats. The aim of the study was to determine if age affected nitric oxide- (NO-) mediated relaxations in normotensive and hypertensive rats. Juvenile (7-week-old) and young adult (22-week-old) male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were used in this study. Femoral artery (FA) reactivity was determined by wire myograph and NO synthase activity by conversion of [3H]-L-arginine. During juvenescence systolic blood pressure (tail-cuff) increased significantly only in SHR, while NO synthesis decreased significantly in both strains. Endothelium-dependent relaxations to acetylcholine were reduced in the FA of SHR compared to age-matched WKY at both ages, yet these parameters were unchanged in adult rats compared with juvenile animals. The NO-dependent component of vasorelaxation was markedly reduced, whereas the NO-independent component was increased in adult compared to juvenile rats in both strains. The endothelial dysfunction in SHR at both ages was associated with reduction of NO-independent mechanisms. In conclusion, aging in early periods of life was associated with reduction of vascular NO production and bioavailability in both strains investigated. This reduction was however fully compensated by accentuation of NO-independent mechanisms.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Age-Related Alterations in Endothelial Function of Femoral Artery in Young SHR and WKY Rats

Púzserová

Ilovska

Bališ

et al. 2014

BioMed Research International

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“…While the exact aetiology of obesity‐related hypertension remains to be determined, the consensus is that elevated sympathetic nerve activity is the main culprit (Hall et al 2010; Lambert et al 2010 b ). Others have suggested that increased total peripheral vascular resistance in hypertension develops due to an imbalance in vasoconstrictor and vasodilator mechanisms (Behuliak et al 2011). Therefore, attenuation of sympathoinhibitory mechanisms may be equally important in the development of obesity‐related hypertension as elevated sympathoexcitatory mechanisms, and evidence for this is emerging (Huber & Schreihofer, 2011).…”

mentioning

confidence: 99%

Renal sympathoinhibitory and regional vasodilator responses to cholecystokinin are altered in obesity‐related hypertension

How

Pumpa

Sartor

2013

Experimental Physiology

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New Findings r What is the central question of this study?The renal and splanchnic circulations command >50% of cardiac output postprandially, and the gut hormone cholecystokinin promotes renal and splanchnic sympathoinhibition and regional vasodilatation. Animals fed a high-fat diet have blunted splanchnic sympathoinhibitory responses to cholecystokinin, but the role of gut peptides has not previously been considered in the aetiology of obesity-related hypertension. r What is the main finding and its importance? Obese, hypertensive animals had blunted renal sympathoinhibitory and renal and mesenteric vasodilator responses to cholecystokinin. These changes may impact cardiovascular homeostasis and lead to increased regional vascular resistance after a meal. Future therapies to treat this condition may include drugs that target the gut.The gut and kidney command >50% of cardiac output postprandially, highlighting the importance of these vascular beds in cardiovascular homeostasis. The gastrointestinal peptide cholecystokinin (CCK) induces vagally mediated splanchnic sympathoinhibition that is attenuated in animals fed a medium high-fat diet (MHFD); therefore, our aim was to determine whether renal sympathetic nerve discharge (RSND) responses to CCK are also affected by this diet, and whether these changes are associated with obesity and hypertension. Another aim was to determine whether regional vasodilator responses to CCK are affected in obesityrelated hypertension. In two separate studies, Sprague-Dawley rats were fed either a low-fat diet (LFD; control) or a MHFD for 13 weeks, after which MHFD animals were classified as obesity prone (OP) or obesity resistant (OR) based on their weight gain falling into the upper or lower tertile, respectively. Arterial pressure and heart rate were monitored in isofluraneanaesthetized, artificially ventilated animals, and either RSND or regional vascular responses to CCK (0.1-8 μg kg −1 ) were evaluated. The OP rats had higher baseline arterial pressure compared with control/OR rats (P < 0.05). Administration of CCK inhibited RSND and increased renal vascular conductance in control/OR rats, and these responses were significantly blunted in OP rats (P < 0.05 for all). Baseline arterial pressure was positively correlated with weight gain and inversely correlated with CCK-induced vasodilatation (P < 0.05 for both). We hypothesize that in obesity-related hypertension, disruption of the sympathoinhibitory signals elicited by CCK reduces vasodilatation in the splanchnic/renal regions, leading to increased postprandial vascular resistance.

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“…Using this model we have shown that chronic pharmacological attenuation of NO synthesis resulted in metabolic alterations and hypertension (Bernatova et al 1996), reduced vasorelaxation and elevated vasoconstriction (Holécyová et al 1996, Bernatova et al 2002b, Pechanova et al 2004a and arterial wall thickening and myocardial fibrosis (Babal et al 1997) in normotensive rats. Moreover, hypertension induced by chronic NOS inhibition in rats seems to be sustained due to interaction of several mechanisms, including the activation of the sympathetic nervous system (including sympatho-adrenomedullary part) and the reninangiotensin system (Sander et al 1995, Zanchi et al 1995, Kvetnansky et al 1997, Gerová et al 2004, Pechanova et al 2004b, Zicha et al 2006, Vargas et al 2007, Zicha et al 2009, Behuliak et al 2011, Paulis et al 2012. Rats subjected to chronic administration of L-NAME are thus a useful experimental tool to study the induction and progression of NO deficiency-mediated endothelial dysfunction and hypertension.…”

Section: Nitric Oxide and Blood Pressure: Involvement Of Enos Nnos Amentioning

confidence: 99%

Blood Pressure Regulation in Stress: Focus on Nitric Oxide-Dependent Mechanisms

Púzserová

Bernátová²

2016

Physiol Res

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Stress is considered a risk factor associated with the development of various civilization diseases including cardiovascular diseases, malignant tumors and mental disorders. Research investigating mechanisms involved in stress-induced hypertension have attracted much attention of physicians and researchers, however, there are still ambiguous results concerning a causal relationship between stress and long-term elevation of blood pressure (BP). Several studies have observed that mechanisms involved in the development of stress-induced hypertension include increased activity of sympathetic nervous system (SNS), glucocorticoid (GC) overload and altered endothelial function including decreased nitric oxide (NO) bioavailability. Nitric oxide is well known neurotransmitter, neuromodulator and vasodilator involved in regulation of neuroendocrine mechanisms and cardiovascular responses to stressors. Thus NO plays a crucial role in the regulation of the stress systems and thereby in the BP regulation in stress. Elevated NO synthesis, especially in the initial phase of stress, may be considered a stress-limiting mechanism, facilitating the recovery from stress to the resting levels via attenuation of both GC release and SNS activity as well as by increased NO-dependent vasorelaxation. On the other hand, reduced levels of NO were observed in the later phases of stress and in subjects with genetic predisposition to hypertension, irrespectively, in which reduced NO bioavailability may account for disruption of NO-mediated BP regulatory mechanisms and accentuated SNS and GC effects. This review summarizes current knowledge on the role of stress in development of hypertension with a special focus on the interactions among NO and other biological systems affecting blood pressure and vascular function.

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Vasodilator efficiency of endogenous prostanoids, Ca2+-activated K+ channels and nitric oxide in rats with spontaneous, salt-dependent or NO-deficient hypertension

Cited by 19 publications

References 35 publications

Age-Related Alterations in Endothelial Function of Femoral Artery in Young SHR and WKY Rats

Age-Related Alterations in Endothelial Function of Femoral Artery in Young SHR and WKY Rats

Renal sympathoinhibitory and regional vasodilator responses to cholecystokinin are altered in obesity‐related hypertension

Blood Pressure Regulation in Stress: Focus on Nitric Oxide-Dependent Mechanisms

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