Decrease In HR Research Articles

Cardiovascular characterization of the DA2 dopamine receptor agonist quinpirole in rats.

In normotensive anesthetized rats, 15-min IV infusions of quinpirole (2.5-40.0 micrograms/kg/min) produced dose-related, rapidly appearing, and long-lasting decreases in mean carotid artery BP and HR. Hemodynamically, the hypotensive effects of quinpirole (10.0 micrograms/kg/min) were due to a fall in total peripheral vascular resistance inasmuch as CO did not undergo significant changes. Mesenteric, hindquarter, and renal blood flows were, respectively, reduced, unchanged, and increased by quinpirole; thus, the renal vascular resistance fell more than either the total peripheral or hindquarter vascular resistance. Biochemically, the hypotensive effects of quinpirole were accompanied by a decrease in the plasma level of norepinephrine and plasma renin activity. The peak fall in blood pressure produced by quinpirole was not significantly modified by atenolol, idazoxan, ranitidine, SCH 23390 (DA1 dopamine receptor antagonist), enalapril, or SK&F 100273 (V1 vasopressin receptor antagonist), but was entirely blocked by S-sulpiride or removal of autonomic nerve drive to the cardiovascular system with chlorisondamine. The effect of quinpirole on systemic and regional vascular resistances was antagonized by S-sulpiride. Furthermore, SK&F 100273 prevented the fall in mesenteric flow produced by quinpirole. Intracerebroventricular injection of quinpirole (10.0 micrograms/kg over 2 min) in saline- or SK&F 100273-pretreated rats produced the same hypotensive effects as an identical IV dose of the compound. In pithed rats, quinpirole (10 micrograms/kg/min IV over 15 min) decreased pressor responses to electrical stimulation of spinal cord outflow without affecting those to exogenously injected angiotensin II, B-HT 920, cirazoline, norepinephrine, or 5-hydroxytryptamine. This inhibitory effect was antagonized by S-sulpiride. The bradycardia produced by quinpirole in intact rats was mediated by the autonomic nervous system inasmuch as it was slightly modified by bilateral vagotomy, partly reduced by atenolol, and entirely prevented by pithing even when the low HR of the last preparation had been raised by IV infusion of isoprenaline. Furthermore, S-sulpiride, but not SCH 23390 or idazoxan, antagonized this effect. In pithed rats, quinpirole similarly inhibited the tachycardic responses elicited by electrical stimulation of either the spinal cord outflow (preganglionic) or postganglionic cardioaccelerator nerve fibers. This effect of quinpirole was susceptible to S-sulpiride but not idazoxan blockade. Finally, in conscious spontaneously hypertensive rats (SHR) but not in normotensive rats, quinpirole (10 micrograms/kg/min IA over 15 min) lowered blood pressure.(ABSTRACT TRUNCATED AT 400 WORDS)

Ｋｅｔａｎｓｅｒｉｎのラット血圧におよぼす影響

Ketanserin, a selective serotonergic (5-HT2) antagonist, also has affinity for alpha 1-adrenoceptors. It is not clear whether the hypotensive mechanism of ketanserin is due to its antagonistic action to 5-HT2 receptor or to its affinity for alpha 1 adrenoceptors. The hypotensive mechanism of ketanserin was studied in both stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY). Anesthetized rats were used (alpha-chloralose + urethane, i.p.). Up to 3 ml of blood was drawn from each rat for analysis. Plasma norepinephrine (NE) was determined by radioenzymatic assay. Plasma serotonin (5-HT) was determined by HPLC-ECD. Adrenal nerve discharges were counted by a digital pulse counter. Ketanserin (0.5 mg/kg, 5.0 mg/kg, i.v.) produced a dose-dependent reduction of mean arterial pressure (MAP) in both SHRSP and WKY. MAP of SHRSP decreased significantly as compared with WKY. Both plasma NE and 5-HT showed a tendency to increase during ketanserin administration (5.0 mg/kg, i.v.). Ketanserin significantly antagonized the BP response induced by exogenously injected 5-HT (30 micrograms/kg) and NE (10 micrograms/kg). Adrenal nerve activity was reduced in parallel with the decrease in BP and HR. These findings suggest that ketanserin produced a decrease in BP via both peripheral and central action in rats.

THE INFLUENCE OF MATERNAL OXYGEN (O2) ADMINISTRATION ON FETAL HEART RATE (FHR) AND LONGTERM VARIABILITY AMPLITUDE (LVA)

02 breathing in healthy adults causes a small decrease in heart rate ( H R ) (2 ) . In healthy fulHerrn infants 02 breathing also leads to a small decrease in HR (1) . When the mother is breathing pure 0 2 , a decrease of FHR and LVA in the fetus can be observed (4) . These observations have been confirmed previously (5). Using an algori thm for Computer determination (CD) of FHR level and LVA (3), i t was the aim of this paper to study the behaviour of FHR and LVA before and during maternal 02 breathing with Computer assistance.

Effects of a warning stimulus on reflex elicitation and reflex inhibition.

ABSTRACTHuman subjects (n = 14) were given a discriminated reaction time task in which the imperative stimulus (IS), a puff of air to the face, was both a signal for a voluntary response and an elicitor of a reflex eyeblink. On one‐half of the trials IS was preceded with a lead time of 100 msec by a stimulus (DS) which both inhibited the reflex blink and served as a signal to refrain from the voluntary response. On one‐half of the trials within each DS‐IS and IS‐alone condition a warning stimulus (WS) led IS by 3000 msec. WS produced a decrease in HR and a faster RT, and WS‐IS trials gave greater reflex amplitudes than IS‐alone trials. Eyeblinks were inhibited by DS and reflex inhibition was more pronounced following the warning stimulus. These data suggest that warning stimuli initiate an attentional process oriented to significant stimuli, thus enhancing both the eliciting and inhibiting functions of these stimuli.

Responses to kayak ergometer performance after kayak and bicycle ergometer training

Ten moderately active male volunteers, age 19-30 years, completed one month of training on either a kayak or a bicycle ergometer (five men in each group). The men completed sixteen 30 minute sessions of continuous work at an intensity which maintained their HR within 85-90% of its maximum, as previously determined on the kayak ergometer. After this training period the kayak group demonstrated significant decreases in VO2, VE, HR and blood lactate in submaximal kayak ergometer work and a significant increase in VO2 during maximal kayak ergometer work. These changes contributed to a significantly higher maximal kayaking work output. The bicycle-trained group did not make any of these improvements on the kayak ergometer. However in their last training session on the bicycle ergometer they were able to work at a higher submaximal load while maintaining the same heart rate as in the first training session. It was concluded that the circulatory and metabolic adjustments to kayak work are greater with kayak training than with bicycle training.