Arterial pressure lability in hypotensive effects of clonidine in barodenervated spontaneously hypertensive rats

Hypotensive effect of clonidine and its effect on arterial pressure lability as the main index of stability of background blood pressure are studied in intact spontaneously hypertensive rats (SHR) and rats with chronic sinoaortic denervation. Barodenervation potentiates hypotensive and negative cardiochronotropic effects of clonidine, which is accompanied by reduced blood pressure lability. This indicates an increased sensitivity of central α₂-and imidazoline receptors, which mediate the depressor effect of clonidine, against the background of chronic inhibition of the baroreceptor reflex. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 9, pp. 295–297, September, 1997     

Ontogenetic dynamics of arterial pressure and ECG in NISAG rats

Ontogenetic changes in cardiac function, relative heart mass, and arterial pressure occurring in rats with genetically determined arterial hypertension (NISAG) are compared with those occurring in normotensive rats (Wistar). In NISAG rats hypertension is accompanied by shift of electrical axis of the heart to the left, increased heart rate, cardiac conductance disturbances, and relative coronary insufficiency. It is suggested that in NISAG rats changes in ECG are secondary to arterial hypertension. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 123, No. 6, pp. 709–713, June, 1997     

Effects of dose and administration mode of endothelin 1 on the mean arterial pressure and heart rate in awake rats

The effects of bolus administration and short-term infusion of endothelin 1 in four doses (2×10⁻¹⁶, 2×10⁻¹⁴, 2×10⁻¹², and 2×10⁻¹⁰ mol/kg) on arterial pressure and heart rate were compared in awake rats. Infusion and bolus administration of the two highest doses increased arterial pressure and provoked bradycardia. Infusion of the two lowest doses increased heart rate without concomitant changes in arterial pressure, while bolus injection of endothelin 1 in the same doses decreased both arterial pressure and the heart rate. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 11, pp. 491–494, November, 1997     

Content of HSP70 in rats with hereditary stress-induced arterial hypertension

Sensitivity of normotensive Wistar rats and NISAG rats (with hereditary arterial hypertension) to heat stress is compared at the organism and cell levels. High temperature sensitivity of NISAG rats correlates with a low content of the main heat shock protein HSP70. This relationship can serve as a biochemical marker of predisposition to arterial hypertension. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 8, pp. 171–173, August, 1997     

Plasma and lymph electrolyte and endocrine parameters in rats with genetically-determined arterial hypertension

Hemolymphatic interactions of electrolytes and plasma contents of aldosterone and insulin are studied in rats with genetically-determined stress-induced arterial hypertension (NISAG) and in normotensive rats (Wistar). Correlation analysis shows that alterations in electrolyte metabolism in NISAG are strongly determined by endocrine influences. These alterations are regarded, on the one hand, as a mechanism responsible for generically-determined arterial hypertension, and, on the other hand, as a variant of “adaptation disease” accompanied by transformation of primarily adaptive reactions into a pathogenic factor of arterial hypertension. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 7, pp. 36–38, July, 1997     

Effect of bombesin (6–14) on arterial pressure in health and in hypovolemic shock

Injection of active fragment of the neuropeptide bombesin (6–14) into cerebral ventricles of intact rabbits induces marked arterial hypertension accompanied by bradycardia and partial redistribution of blood to specialized heat-emitting organs (auricular conchae), which reduces body temperature. After a considerable blood loss, the peptide normalizes arterial pressure without affecting cardiac activity and body temperature. It is suggested that bombesins may be used for compensation of arterial hypotension during the early period of hypovolemic shock. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 122, No. 10, pp. 372–374, October, 1996     

Changes in baroreceptor vagal reflex performance in the developing rat

 Ontogenesis of both vagal control of heart rate and the baroreceptor vagal reflex were evaluated in rats at postnatal ages (P) of 5/6, 10, 15, 20, 25 and >42 days anaesthetised with urethane (1.5 g/kg). Between P5/6 and P25 heart rate rose from 372 ± 12 to 448 ± 20 beats per minute and mean arterial pressure increased from 33.9 ± 3.1 to 74.59 ± 3.25 mm Hg (mean ± SEM, n = 7 and 11 respectively). Cardiac vagal tone was absent at P10 but significant at P20 (P < 0.05) as revealed with atropine (0.5–1 mg/kg i.v.). Baroreceptor cardiac reflex sensitivity, tested with phenylephrine (10–50 μg/kg i.v.), was attenuated significantly in P10–20 rats compared with P5/6, P25 and mature animals. In P14–17 rats stimulation of neurones in either the solitary tract or ambiguual nuclei, by microinjection of L-glutamate (100–200 pmol), evoked an atropine-sensitive bradycardia indicating a functional integrity of central and peripheral efferent pathways mediating the baroreceptor reflex. Thus, the baroreceptor vagal reflex is functional in P5/6 rats but becomes attenuated between P10–P20, which is coincident with the maturational rise in arterial pressure. Received: 8 January 1997 / Received after revision: 26 March 1997 / Accepted: 14 April 1997     

Comparative analysis of effects from prolonged peripheral and intracerebral administrations of angiotensin II in rats

Variations in arterial pressure and food and water consumption were studied in rats during and after their prolonged continuous exposure to angiotensin II using osmotic minipumps. Subcutaneously administered angiotensin-II (300 μg over 7 days) induced long-lasting hypertension followed by hypotension. Angiotensin-II administered into a lateral cerebral ventricle (3 μg over the same period) led to a significant fall in arterial pressure. The peripheral and intracerebral angiotensin-II administrations were both accompanied by increased water consumption. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N^no 10, pp. 352–354, October, 1994 Presented by K. V. Sudakov, Member of the Russian Academy of Medical Sciences     

Role of ATP as a sympathetic nervous system transmitter in the smoothing of rapid arterial pressure changes

Arterial pressure lability and its variations were examined in unrestrained rats following selective elimination of adrenergic or purinergic sympathetic influences on the circulatory system. Both the α₁-andrenoceptor blocker prazosin and the nonselective α-adrenoceptor blocker phentolamine lowered the arterial pressure without affecting its lability. When P_2x purine receptors were desensitized with α,β-methyleneATP, the resulting pronounced hypotension was accompanied by a two-fold increase in the lability of mean arterial pressure. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 120, N^no 11, pp. 461–464, November, 1995 Presented by I. P. Ashmarin, Member of the Russian Academy of Medical Sciences     

Adaptation to periodic high-altitude hypoxia inhibits baroreflex vagal bradycardia in rats

A 3-week course of adaptation to high-altitude hypoxia (4500 m above sea level) inhibited baroreflex avagal bradycardia induced by a rapid rise of systemic blood pressure in conscious rats. Bradycardic responses to electrical stimulation of peripheral end of the right vagus nerve and methacholine (M₂ muscarinic receptor agonist) in hypoxia-adapted rats did not differ from the control. It is concluded that hypoxia inhibits baroreflex vagal bradycardia by acting on a central element of the baroreceptor reflex arch Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 129, No. 4, pp. 386–389, April, 2000     

Signalling across the blood brain barrier by angiotensin II: novel implications for neurogenic hypertension

Angiotensin II (AngII) is a major culprit in essential hypertension. Based on a genetic rodent model of hypertension, we review here evidence that AngII may signal across the blood brain barrier to affect neuronal circuits within the nucleus tractus solitarii (NTS) of the brainstem, a pivotal region regulating both the baroreceptor reflex and set point control of arterial pressure. We have termed this form of signalling as vascular–neuronal signalling. We describe that the depressant action of AngII in NTS on the baroreceptor reflex is mediated via activation of endothelial nitric oxide synthase (eNOS) releasing NO that promotes release of the inhibitory transmitter—GABA. This could shunt the incoming excitatory baroreceptor afferent traffic impinging on NTS neurones. Chronic studies recording arterial pressure in conscious unrestrained rats using radio-telemetry have revealed that eNOS in NTS plays an endogenous physiological role in the homeostatic regulation of the gain of the cardiac baroreceptor reflex. However, in the spontaneously hypertensive rat, eNOS mRNA was higher (compared to normotensive rats), and its chronic blockade in NTS restored the abnormally depressed cardiac baroreceptor reflex to levels akin to normotensive rats, improved heart rate variability and lowered arterial pressure. Hence, it seems that excessive eNOS activity in NTS of the SHR contributes to the pathological state of this animal model’s cardiovascular autonomic nervous system. We speculate on why eNOS activity may be up regulated in the NTS of the SHR and propose that it is a consequence of high cerebral vascular resistance and inadequate blood perfusion of the brainstem.     

Myocardial hypertrophy of the left ventricle during familial arterial hypertension

In patients with familial arterial hypertension and their relatives preclinical signs of myocardial hypertrophy were observed before the formation of stably increased blood pressure. We evaluated echocardiographic sings of left ventricular myocardial hypertrophy in normotensive relatives of patients with arterial hypertension. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 140, No. 12, pp. 625–626, December, 2005     

Specific response to adrenaline in arterial hypertension induced by exogenous calcium deficiency

Injection of a synthetic analog of parathyroid hypertensive factor to WKY rats considerably increases and prolongs pressor response to adrenaline. Synthetic analog injected after adrenaline induces a short-term (3–4 min) and potent (to 250%) rise of arterial pressure. Each subsequent injection of the synthetic analog induces a less pronounced in the amplitude and duration pressor response. The α-adrenoblocker phentolamine completely abolishes the effects of the parathyroid hypertensive factor analog. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 8, pp. 148–150, August, 1997     

Vasoconstriction reactions in tail artery in the rats with regional arterial hypotension

Reactivity of the tail artery to norepinephrine was studied in rats with regional arterial hypotension. Constant-flow perfusion of the artery elicited less pronounced constriction in hypotensive rats in comparison with the controls, while the constant-pressure perfusion evoked stronger vasoconstriction. This is explained by possible involvement of myogenic component in the contractile response. When myogenic reaction was inhibited by enhanced potassium concentration in the perfusion solution, vasoconstriction in hypotensive rats was less pronounced under both perfusion modes. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 1, pp. 11–13, January, 1999     

Changes in gluco- and mineralocorticoid adrenal functions in spontaneously hypertensive rats during experimental myocardial infarction

The dynamics of corticosterone and aldosterone contents during the acute and restoration periods of experimental myocardial infarction was studied in Wistar and spontaneously hypertensive rats. In spontaneously hypertensive rats, the increase in aldosterone concentration during the acute period was followed by elevation of corticosterone content, which attested the disadaptive course of experimental myocardial infarction against the background of hereditary arterial hypertension. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 129, No. 1, pp. 25–27, January, 2000     

The cause of the difference between the arterial baroreceptor reflex under natural pulsatile circulation and under nonpulsatile systemic circulation

In a previous study we investigated the relation between afferent and efferent activity of the arterial baroreceptor reflex under nonpulsatile systemic circulation using total left heart bypass. The results indicated that the regulation of the arterial baroreceptor reflex was converted under nonpulsatile systemic circulation, and we inferred that a possible reason for this conversion was the transformation in discharge of the afferent activity of the arterial baroreceptor reflex that took place under nonpulsatile systemic circulation. In the present study we tested this hypothesis by sectioning carotid sinus and aortic depressor nerves and electrically stimulating bilateral aortic depressor nerves under anesthesia in five rabbits (400 spikes for 20s, with 0.02ms pulse width and 8 V amplitude), while recording changes in aortic pressure, mean aortic pressure, and heart rate. Continuous stimulation was taken as discharge of the afferent activity of the arterial baroreceptor reflex under nonpulsatile systemic circulation, and periodic stimulation was taken as discharge under natural pulsatile circulation. Aortic pressure, mean aortic pressure, and heart rate decreased under both continous and periodic stimulation. The decreases in mean aortic pressure and heart rate during continuous stimulation were significantly lower than those during periodic stimulation. Our results suggest that the transformation in discharge of the afferent activity of the arterial baroreceptor reflex under nonpulsatile systemic circulation may have played an important causative role in the conversion of the regulation of the arterial baroreceptor reflex under nonpulsatile systemic circulation.     

Peculiarities of active avoidance conditioning in rats with various forms of inherited arterial hypertension

Peculiarities of active avoidance conditioning were studied in NISAG rats (hereditary stress-induced arterial hypertension) and spontaneously hypertensive SHR rats. Conditioning was successful in 90% normotensive Wistar rats and in only 9.1% NISAG rats. Hypertensive SHR rats were intermediate between Wistar and NISAG rats by their learning capacity (66.7%). Our results suggest that differences in learning capacity of hypertensive rats are determined by genetic characteristics of animal behavior and emotional state, rather than blood pressure elevation. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 142, No. 10, pp. 386–388, October, 2006     

Nonopioid nature of the pressor effect of FMRF-amide

The effect of the peptide FMRFa on arterial pressure, heart rate, and respiratory rate is examined in anesthetized rats. It is demonstrated that the effect of FMRFa is similar to that of epinephrine and is characterized by transient hypertension against the background of bradycardia and decreased respiratory rate followed by hypotensive phase. Opiate antagonists and agonists do not modify the effect of FMRFa. Pressor effect of FMRFa is inhibited by Aminazine and is abolished by dihydroergotamine, while clopheline, reserpine, propranolol, Dimedrol, and adrenalectomy have no appreciable effect on it. It is suggested that the effects of FMRFa are realized via vascular adrenoreceptors. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 11, pp. 513–515, November, 1997     

State of the myocardium in rats of a new hypertensive strain

Study of the heart in a new strain of rats with hereditary stress-induced hypertension (NISAG) reveals a complex of structural and functional changes which are analogous to the manifestations of essential hypertension. These changes are shown to be adaptive-compensatory in nature and indicative of limited functional reserves of the hypertrophic myocardium. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 122, No. 9, pp. 271–273, September, 1996     

Mechanism of arterial pressure elevation in calcium deficiency

We compared the effects of intravenous administration of the calcium-dependent hypertensive factor from the plasma of patients with essential hypertension and of a synthetic heptapeptide with hypertensive activity. Both substances prove to induce prolonged and pronounced elevation of arterial blood pressure. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 117, N ^o 5, pp. 476–477, May, 1994 Presented by A. N. Klimov, Member of the Russian Academy of Medical Sciences