PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 9328607

Evidence for genetic variability in venous responsiveness.

Z Vajo·B Székács·W Dachman
View original source ↗Export metadata ↓

Abstract

Alterations in adrenergic mediated vascular responsiveness and glucose metabolism have been implicated in the pathogenesis of essential hypertension. We sought for a human model to study possible interactions between the two pathogenetical factors. In a group of Latin-Americans there is a predominance of diabetes mellitus, impaired glucose tolerance and obesity, while the rate of hypertension is unexpectedly low (lower than in the normal population). Here we demonstrate attenuated alpha 1 adrenergic mediated vasoconstriction in the above group, suggesting a possible protective mechanism against the development hypertension.

Explore related subjects

Adrenergic alpha-AgonistsAdultDose-Response Relationship, DrugFemaleGeneticsGlucoseHandHumansMaleMuscle, Smooth, VascularPhenylephrineRegional Blood FlowSympathetic Nervous SystemVasodilationVeinsClinical TrialJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Z Vajo, B Székács, W Dachman. 1996. Evidence for genetic variability in venous responsiveness.. https://pubmed.ncbi.nlm.nih.gov/9328607/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Dexmedetomidine-induced pulmonary alterations in sheep.

Alpha(2) agonist-induced pulmonary oedema in sheep might be related to alterations in pulmonary haemodynamics and/or activation of inflammatory processes. In seven sevoflurane-anaesthetized sheep pulmonary haemodynamics, arterial oxygen tensions, nitric oxide and prostaglandin E(2) concentrations were determined before and after intravenous dexmedetomidine (2microg kg(-1)). In a second trial, lung tissue was sampled for histopathology and quantitative real-time PCR for IL-1beta and iNOS mRNA in a control sheep and 2, 10 and 30min after dexmedetomidine. Computer tomography of the lung under sevoflurane anaesthesia before and after dexmedetomidine was performed. Two minutes after dexmedetomidine mean pulmonary artery pressure, pulmonary arterial occlusion pressure and estimated capillary pressurewere significantly increased to 34.5mmHg, 22.2mmHg and 27.1mmHg, respectively. On computer tomography, lung density increased immediately after dexmedetomidine, with maximal density occurring between 9 and 12min. Histopathology was consistent with vascular congestion followed by protein and erythrocyte extravasation into alveoli. Increased iNOS mRNA levels were detected in sevoflurane anaesthetized animals only. An IL-1beta signal occurred after morphological changes had occurred in lung tissue. These findings support hydrostatic stress as the underlying cause of alpha(2) agonist-induced pulmonary oedema in sheep.

Adrenergic alpha-Agonists↗
PubMed2007

Presynaptic alpha-adrenoceptors in median preoptic nucleus modulate inhibitory neurotransmission from subfornical organ and organum vasculosum lamina terminalis.

The median preoptic nucleus (MnPO) in the lamina terminalis receives a prominent catecholaminergic innervation from the dorsomedial and ventrolateral medulla. The present investigation used whole cell patch-clamp recordings in rat brain slice preparations to evaluate the hypothesis that presynaptic adrenoceptors could modulate GABAergic inputs to MnPO neurons. Bath applications of norepinephrine (NE; 20-50 microM) induced a prolonged and reversible suppression of inhibitory postsynaptic currents (IPSCs) and reduced paired-pulse depression evoked by stimulation in the subfornical organ and organum vasculosum lamina terminalis. These events were not correlated with any observed changes in membrane conductance arising from NE activity at postsynaptic alpha(1)- or alpha(2)-adrenoceptors. Consistent with a role for presynaptic alpha(2)-adrenoceptors, responses were selectively mimicked by an alpha(2)-adrenoceptor agonist (UK-14304) and blockable with an alpha(2)-adrenoceptor antagonist (idazoxan). Although the alpha(1)-adrenoceptor agonist cirazoline and the alpha(1)-adrenoceptor antagonist prazosin were without effect on these evoked IPSCs, NE was noted to increase (via alpha(1)-adrenoceptors) or decrease (via alpha(2)-adrenoceptors) the frequency of spontaneous and tetrodotoxin-resistant miniature IPSCs. Collectively, these observations imply that both presynaptic and postsynaptic alpha(1)- and alpha(2)-adrenoceptors in MnPO are capable of selective modulation of rapid GABA(A) receptor-mediated inhibitory synaptic transmission along the lamina terminalis and therefore likely to exert a prominent influence in regulating cell excitability within the MnPO.

Adrenergic alpha-Agonists↗