Plasma Neuropeptide Y and Catecholamines in Women and Men with Essential Hypertension

Wocial, B; Ignatowska-Switalska, H; Pruszczyk, Piotr; Jędrusik, Piotr; Januszewicz, Andrzej; Łapiński, M; Januszewicz, W; Zukowska‐Grojec, Zofia

doi:10.3109/08037059509077586

Cited by 32 publications

(25 citation statements)

References 28 publications

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“…In contrast to leptin, NPY is a very potent stimulant of appetite [22,23]. On the other hand, NPY is a potent vasoconstrictor and is presumed to be involved in the pathogenesis of essential hypertension [25][26][27][28]. As was shown in the present study, EHP showed elevated plasma NPY concentrations.…”

Section: Discussionsupporting

confidence: 67%

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Does Leptin Play a Role in the Pathogenesis of Essential Hypertension?

Kokot

Adamczak²,

Wiȩcek³

et al. 1999

Kidney Blood Press Res

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Background: Leptin is produced and released by adipocytes in proportion to fat stores. Leptin as an anorectic hormone plays an important role in the regulation of food intake, energy expenditure, and insulin secretion. In contrast, neuropeptide Y, insulin, cortisol, and growth hormone are presumed to be appetite modulators. Leptin and neuropeptide Y are both involved in the activation of sympathetic tone. Increased body fat stores in obese patients are involved in the pathogenesis of some metabolic disorders (e.g., hyperinsulinaemia, glucose intolerance) and arterial hypertension. Methods and Results: Based on this pathophysiological background, we tried to assess the relationship between plasma leptin and blood pressure in 41 patients with essential hypertension (EHP; 20 females, 21 males, mean age 38.7±1.9 years, mean body mass index – BMI – 25.8±0.5 kg/m²) and in an appropriately sex– and BMI–matched control group of 27 normotensive healthy subjects (NHS; 11 females, 16 males, mean age 39.7±2.5 years, mean BMI 24.8±0.6 kg/m²). The plasma leptin concentration did not differ significantly between EHP and NHS (13.0±1.9 vs. 8.1±1.0 ng/ml, respectively). In both groups a significant positive correlation was found between BMI and plasma leptin concentration (p<0.0001). A significant positive correlation (p<0.02) was found between leptinaemia and mean (MAP), systolic and diastolic blood pressures, if data were analyzed for all examined subjects or separately only for women. Such a correlation could not be confirmed for male NHS and EHP subjects. The plasma neuropeptide Y concentration was higher in EHP than in NHS (77.1±23.0 vs. 63.6±9.8pg/ml, p = 0.05). In contrast to neuropeptide Y plasma insulin, cortisol, and growth hormone concentrations were similar in EHP and in NHS. Conclusion: Both EHP and NHS are characterized by a positive correlation between BMI and leptinaemia. Leptin may be indirectly involved in blood pressure regulation, especially in women of both NHS and EHP.

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Section: Discussionsupporting

confidence: 67%

“…NPY exerts a vasoconstrictor action and potentiates noradrenaline and angiotensin II induced contraction of vascular myocytes [25,26]. Therefore, NPY may play a role in the pathogenesis of essential hypertension [27,28]. It was also found, that glucocorticoids stimulate leptin secretion under both experimental [29] and clinical [30,31] conditions.…”

mentioning

confidence: 96%

Does Leptin Play a Role in the Pathogenesis of Essential Hypertension?

Kokot

Adamczak²,

Wiȩcek³

et al. 1999

Kidney Blood Press Res

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“…It has been established that the receptor responsible for the vasoconstrictor effects of NPY in cat skeletal muscle is the NPY-Y 1 receptor (9). NPY has been implicated in hypertension (22) with high circulating levels in both men and women with the disease (38). Moreover, the mitogenic potential of NPY has been established (29,34,40,41).…”

mentioning

confidence: 98%

Y₁- and α₁-receptor control of basal hindlimb vascular tone

Jackson

Noble

Shoemaker

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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The role of endogenous Y(1)-receptor activation on skeletal muscle vasculature under baseline conditions is currently debated and no in vivo studies have been performed to address this issue. Therefore, this study was designed to address the effect of Y(1)-receptor and/or alpha(1)-adrenoceptor antagonism on basal hindlimb vascular conductance in male Sprague-Dawley rats in vivo. Left hindlimb vascular conductance, carotid artery mean arterial pressure, and heart rate were measured during low volume infusion of N(2)-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-d-arginine amide (BIBP3226; 100 microg/kg), prazosin (20 microg/kg), and combined blockade to the left hindlimb. Vascular conductance increased 1.5 +/- 0.5 microl.min(-1).mmHg(-1) with BIBP3226 infusion, 1.7 +/- 0.5 microl.min(-1).mmHg(-1) with prazosin infusion, and 4.8 +/- 1.0 microl.min(-1).mmHg(-1) with combined blockade (P < 0.05). Interestingly, systolic vascular conductance increased in all three conditions, but diastolic vascular conductance only increased in the two conditions where BIBP3226 was present. These data indicate that Y(1)-receptor activation plays an important role in the regulation of vascular conductance in the resting rat hindlimb. Furthermore, this effect was of the same magnitude as the alpha(1)-adrenoceptor contribution. The differential flow profiles following alpha(1) blockade with and without Y(1)-receptor blockade supports local differences in receptor distribution.

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“…It is also likely NPY is involved in the pathogenesis of hypertension [7], since plasma concentrations of NPY are elevated in both hypertensive men and women compared to normotensive subjects [8, 9]. Moreover, in SHR NPY-containing nerve density appears increased in the cerebral and mesenteric vasculature [10, 11], although the content is decreased in the heart and kidney [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Enhanced Neuropeptide Y Immunoreactivity and Vasoconstriction in Mesenteric Small Arteries from Spontaneously Hypertensive Rats

Gradin

Li²,

Andersson³

et al. 2003

J Vasc Res

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Enhanced sympathetic nerve activity is thought to play a role in the pathogenesis of hypertension. The purpose of the present study was to investigate the mechanisms underlying the enhanced vasocontractile response to perivascular stimulation of mesenteric arteries isolated from female spontaneously hypertensive rats (SHR). Innervation of mesenteric small arteries was evaluated by immunohistochemistry and confocal microscopy while functional studies were conducted in a microvascular myograph. The distribution of nerve terminals immunoreactive for tyrosine hydroxylase (TH) and neuropeptide Y (NPY) was similar in mesenteric small arteries from Wistar-Kyoto (WKY) and SHR rats. However, immunointensity of TH or NPY immunoreactivities were much higher in small arteries from SHR compared to WKY. Expressed as percentage of contractions elicited by 124 mM K⁺, concentration-response curves for noradrenaline (NA) and NPY were shifted leftward in SHR compared with WKY rats. The combination of noradrenaline (1 µM) and NPY (10 nM) contracted mesenteric arteries from WKY and SHR to higher levels than compared to either contractile agent added alone. The NPY Y₁ receptor antagonist, BIBP 3226, inhibited these contractions with 87 ± 0.7 and 80 ± 1.3% (p < 0.05, n = 6) in arteries from WKY and SHR rats, respectively. In arteries incubated with the α₁-adrenoceptor antagonist, prazosin, and preactivated with vasopressin, electrical field stimulation evoked contractions which were more pronounced in mesenteric arteries from SHR compared to WKY rats. BIBP 3226 partially inhibited these contractions. In vasopressin-activated arteries BIBP 3226 caused rightward shifts of the concentration-response curves for NPY in mesenteric arteries from SHR rats, but in addition it also abolished the maximal NPY contraction in arteries from WKY rats. In the presence of BIBP 3226, low concentrations (1 pM to 10 nM) of NPY caused relaxations in arteries from WKY, but not in segments from SHR rats. Mechanical removal of the endothelium abolished NPY relaxation in arteries from WKY. In arteries activated with vasopressin and exposed to either forskolin or sodium nitroprusside, the addition of NPY evoked contractions which were more pronounced in arteries from SHR compared to WKY arteries. The present study suggests that enhanced NPY content and vasoconstriction to NPY in arteries from hypertensive rats can contribute to the enhanced sympathetic nerve activity and vascular resistance in female hypertensive rats. Endothelial cell dysfunction as well as alterations in smooth muscle response to NPY seem to contribute to the enhanced vasoconstriction in arteries from hypertensive animals.

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Plasma Neuropeptide Y and Catecholamines in Women and Men with Essential Hypertension

Cited by 32 publications

References 28 publications

Does Leptin Play a Role in the Pathogenesis of Essential Hypertension?

Does Leptin Play a Role in the Pathogenesis of Essential Hypertension?

Y₁- and α₁-receptor control of basal hindlimb vascular tone

Enhanced Neuropeptide Y Immunoreactivity and Vasoconstriction in Mesenteric Small Arteries from Spontaneously Hypertensive Rats

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Plasma Neuropeptide Y and Catecholamines in Women and Men with Essential Hypertension

Cited by 32 publications

References 28 publications

Does Leptin Play a Role in the Pathogenesis of Essential Hypertension?

Does Leptin Play a Role in the Pathogenesis of Essential Hypertension?

Y1- and α1-receptor control of basal hindlimb vascular tone

Enhanced Neuropeptide Y Immunoreactivity and Vasoconstriction in Mesenteric Small Arteries from Spontaneously Hypertensive Rats

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Product

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Y₁- and α₁-receptor control of basal hindlimb vascular tone