The role of central vasopressin V2 receptors in cardiovascular homeostasis

[S. M. Milutinović-Smiljanić]

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Neuronauke - neurokardiologija / Neuroscience - neurocardiology

Poznato je da vazopresin modulira nervnu regulaciju kardiovaskularnog sistema centralno i periferno, ali tačan mehanizam još uvek je nepoznat. Da bi ispitali da li centralni V2 receptori vazopresina modifikuju nervnu regulaciju kardiovaskularnog sistema ispitivali smo efekte centralno ubrizganog selektivnog antagoniste V2 receptora na hemodinamske parametre: krvni pritisak, srčanu frekvenciju i njihov varijabilitet, pod bazalnim fiziološkim uslovima i u stresu. Pored toga, pod bazalnim fiziološkim uslovima ispitali smo efekat hiperekspresije V2 receptora u paraventrikularnom jedru hipotalamusa na hemodinamske parametre neanestetisanog pacova. Krvni pritisak i srčana frekvencija registrovani su direktnom metodom preko katetera postavljenog u femoralnu arteriju ili radiotelemetrijskog transmitera u aortu. Nervna regulacija krvnog pritiska i srčane frekevencije evaluirana je spektralnom metodom. Pod bazalnim fiziološkim uslovima antagonist V2 vazopresinskih receptora nije modifikovao krvni pritisak i srčanu frekvenciju, ali je izazvao porast oscilacija veoma niskih frekvencija krvnog pritiska. Hiperekspresija V2 receptora u paraventrikularnom jedru hipotalamusa pacova izazvala je porast niskofrekventnog varijabiliteta simpatičkog porekla kako u krvnom pritisku, tako i u srčanoj frekvenciji. Stres izazvan mlazom vazduha pod pritiskom usmeren u potiljak pacova prouzrokovao je istovremeni porast krvnog pritiska i srčane frekvencije, kao i njihovog niskofrekventnog varijabiliteta simpatičkog porekla i visokofrekventnog varijabiliteta respiratornog porekla. Pacovi pretretirani antagonistom V2 receptora i potom izlagani stresu ispoljili su manji skok krvnog pritiska i varijabiliteta simpatičkog i respiratornog porekla, kao i kraći oporavak. Rezultati pokazuju da vazopresin putem stimulacije centralnih V2 receptora utiče na kardiorespiratorni odgovor na stres.

It is well established that vasopressin modulates neurogenic control of the circulation both centrally and peripherally. However the exact mechanism is still unexplored. To investigate whether central V2 receptors modulate the neurogenic control of the circulation, we studied the effects of centrally injected selective V2 antagonist on hemodynamic parameters: blood pressure (BP), heart rate (HR) and their variability, under baseline physiological conditions and during stress. We also investigated the effects of over-expression of V2 receptors in the paraventricular nucelus of the hypothalamus on cardiovascular hemodynamic under baseline conditions. BP and HR were assessed by direct recording via indwelling catheter in femoral artery or by radiotelemetric probe inserted in abdominal aorta. Neurogenic control of the circulation was assessed by spectral methodology. Under baseline physiological conditons V2 antagonist didn't modify the level of BP and HR and increased the very low frequency variability of BP. Over-expression of V2 receptors in the paraventricular nucleus increased sympathetically mediated, low-frequency oscillation of BP and HR. Exposure of rats to air-jet stress increased BP, HR and their sympahtetically mediated low-frequency variability and respiration-induced high-frequency variability. Rats pre-treated with the V2 antagonist and exposed to stress exhibited lower BP increase and lower increase od BP variability, as well as shorter recovery time. It follows that vasopressin by the stimulation of central V2 receptors influence the cardiorespiratory response to stress.

vazopresin, V2, stres, paraventrikularno jedro hipotalamusa, krvni pritisak, srčana frekvenca, varijabilitet

vasopressin, V2, stress, hypothalamus, blood pressure, heart rate, cardiovascular variability

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