Nervous control of heart rate: activity in the cardiac vagus of the dogfish

1982 ◽  
Vol 53 (6) ◽  
pp. 1330-1335 ◽  
Author(s):  
E. W. Taylor ◽  
P. J. Butler
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Action Potentials ◽  
Sympathetic Innervation ◽  
Nervous Control ◽  
Temporal Relationships ◽  
Maximum Water ◽  
External Stimuli ◽  
Neurophysiological Basis ◽  
Stimulation Of

In the absence of any sympathetic innervation to the heart, nervous control of heart rate in the dogfish is solely attributable to inhibitory parasympathetic input from the vagus nerve. Action potentials can be recorded from the cardiac vagus of the dogfish following its exposure in the anterior cardinal sinus. The rates of heartbeat and ventilation, blood pressure, hematocrit, and responses to external stimuli such as hypoxia, which include a bradycardia, remained typical of fish with their nervous and circulatory systems virtually intact. The recordings included sporadically active units that accelerated during hypoxia, possibly inducing the bradycardia, and regular bursts of action potentials synchronous with ventilatory movements that appeared to arise reflexly from stimulation of pharyngeal proprioceptors. These bursts may loosely couple the respiratory and cardiac pumps, increasing the probability of concurrence between periods of maximum water and blood flow. The preparation enables detailed study of the temporal relationships between the pumps and its neurophysiological basis.

Temporal relationships of barosensory attenuation in conscious rabbits

1976 ◽  
Vol 230 (6) ◽  
pp. 1480-1486 ◽  
Author(s):  
MP Gimpl ◽  
AL Brickman ◽  
MP Kaufman ◽  
N Schneiderman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Hypothalamic Stimulation ◽  
Aortic Nerve ◽  
Temporal Relationships ◽  
Train Stimulation ◽  
Posterior Hypothalamic Stimulation ◽  
Simple Summation ◽  
Stimulation Of

Electrical stimulation of anterior or posterior hypothalamus with 10-s trains elicited heart rate and blood pressure decreases. Presentation of anterior hypothalamic stimulation coincident with or 5, 10, or 15 s prior to 5-s train stimulation of aortic nerve (AN) summated with depressor-decelerator responses to AN stimulation. The summating effect was more pronounced for heart rate than for blood pressure. Simultaneous onset of AN and posterior hypothalamic stimulation did not influence AN responses. In contrast, when AN stimulation was delayed until 5, 10, or 15 s after onset of posterior hypothalamic stimulation, small, moderate, and full attenuation of AN responses occurred, respectively. Since AN and posterior hypothalamic stimulation each led to depressor-decelerator responses, attenuation of AN responses cannot be attributed to simple summation of cardiovascular responses elicited by intracranial and aortic nerve stimulation.

Cardiovascular responses to head-stand posture

1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
High Pressure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Skin Temperature ◽  
Cardiovascular Responses ◽  
Posterior Tibial Artery ◽  
Nervous Control ◽  
Posterior Tibial

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Impaired baroreflex control of vascular resistance in prehypertensive Dahl S rats

1983 ◽  
Vol 245 (2) ◽  
pp. H210-H217 ◽  
Author(s):  
F. J. Gordon ◽  
A. L. Mark
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Strain Difference ◽  
Sympathetic Innervation ◽  
Baroreflex Control ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Elevated Arterial Pressure

The purpose of this study was to examine baroreflex control of vascular resistance and heart rate in prehypertensive Dahl salt-sensitive (DS) and salt-resistant (DR) rats. Urethan-anesthetized normotensive DS rats demonstrated significantly impaired baroreflex control of both hindlimb vascular resistance and heart rate. This impairment was not secondary to elevated arterial pressure since blood pressure did not differ between DR and DS rats fed a low sodium diet. Vascular baroreflex responses were shown to depend on the integrity of efferent sympathetic innervation and to be mediated by the sinoaortic afferent arterial baroreceptors. No strain difference was observed for hindlimb vasodilation produced by papaverine or graded doses of nitroprusside, indicating that differences in resistance vessel vasodilator capacity or responsiveness could not account for differences in baroreflex responses. Since impaired baroreflex control was evident in DS rats prior to any elevation in arterial pressure, this abnormality may contribute to the DS rat's genetic propensity to develop hypertension.

SOME RESPIRATORY AND CARDIOVASCULAR EFFECTS OF GRADUAL SARIN POISONING IN THE RAT

1961 ◽  
Vol 39 (6) ◽  
pp. 1001-1011 ◽  
Author(s):  
W. C. Stewart ◽  
D. H. McKay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Gastrocnemius Muscle ◽  
Artificial Ventilation ◽  
Cardiovascular Effects ◽  
Vagus Nerves ◽  
Toxic Dose ◽  
Circulatory Insufficiency ◽  
Slow Intravenous Infusion ◽  
Stimulation Of

Anesthetized rats were given sarin (isopropyl methylphosphonofluoridate) by slow intravenous infusion, while respiration, blood pressure, heart rate, and contractions of the gastrocnemius muscle in response to stimulation of the sciatic nerve were recorded.When artificial ventilation was not carried out, breathing stopped after a toxic dose of sarin had been given, even though the blood pressure was above normal and neuromuscular conduction was not impaired. On the other hand, when artificial ventilation was provided after breathing stopped, the blood pressure and heart rate fell, and death was apparently caused by circulatory insufficiency.Infusion of sarin caused slowing of the heart rate which was not prevented by previous section of the vagus nerves. Injection of atropine restored the heart rate to normal, and enabled the animals to withstand large doses of sarin as long as artificial ventilation was maintained.It was concluded that sarin caused a cholinergic circulatory collapse which was the cause of death in rats maintained with artificial ventilation. This circulatory insufficiency was alleviated by large doses of atropine. Possible causes of the depression of circulation are discussed, and reasons are given for believing it to be due mainly to cholinergic diminution of cardiac output, caused by accumulation of acetylcholine in the heart.

Adenosine as a mediator of macula densa-dependent inhibition of renin secretion

2006 ◽  
Vol 290 (5) ◽  
pp. F1016-F1023 ◽  
Author(s):  
Soo Mi Kim ◽  
Diane Mizel ◽  
Yuning G. Huang ◽  
Josie P. Briggs ◽  
Jurgen Schnermann
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin ◽  
Macula Densa ◽  
Renin Secretion ◽  
Nacl Transport ◽  
Dependent Inhibition ◽  
Deficient Mice ◽  
Stimulation Of

Adenosine acting through A1 adenosine receptors (A1AR) has been shown previously to be required for the vasoconstriction elicited by high luminal NaCl concentrations at the macula densa (MD). The present experiments were performed to investigate a possible role of A1AR in MD control of renin secretion in conscious wild-type (WT) and A1AR-deficient mice. The intravenous injection of NaCl (5% body wt) reduced plasma renin concentration (PRC; ng ANG I·ml−1·h−1) from 1,479 ± 129 to 711 ± 77 ( P < 0.0001; n = 18) in WT mice but did not significantly change PRC in A1AR−/− mice (1,352 ± 168 during control vs. 1,744 ± 294 following NaCl; P = 0.19; n = 17). NaCl injections also caused a significant reduction in PRC in β1/β2-adrenergic receptor−/− mice (298 ± 47 vs. 183 ± 42; P = 0.03; n = 6). Injections of isotonic NaHCO3 (5% body wt) elicited significant increases in PRC in both WT and A1AR−/− mice. NaCl as well as NaHCO3 injections were accompanied by transient increases in blood pressure, heart rate, and activity that were similar in WT and A1AR−/− mice. The increase in PRC caused by an intraperitoneal injection of furosemide (40 mg/kg) was comparable in WT and A1AR−/− mice, and it was accompanied by similar transient increases in blood pressure, heart rate, and activity. Similarly, the stimulation of PRC caused by hydralazine was the same in WT and A1AR−/− mice. We conclude that the inhibition of renin secretion in response to an increase in NaCl at the MD requires A1AR and therefore appears to be adenosine dependent, whereas the stimulation of renin secretion during reductions in MD NaCl transport or arterial pressure does not require functional A1AR.

Beta2-mediated hypotension and myocardial injury

1982 ◽  
Vol 60 (8) ◽  
pp. 1144-1148 ◽  
Author(s):  
Alison Brown-Lukacsko ◽  
Peter Lukacsko
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Myocardial Injury ◽  
Elevated Serum ◽  
Blocking Agent ◽  
Arterial Blood ◽  
Ganglionic Blocking ◽  
Elevated Heart Rate ◽  
Stimulation Of

This study was designed to investigate the importance of beta2 receptor mediated hypotension in the pathogenesis of myocardial injury. The effect of isoproterenol and the putative beta2 agonist albuterol on arterial blood pressure, heart rate, the myocardial content of ATP and cAMP, and the serum content of MB-CPK was examined in conscious rats. Isoproterenol (5.25 mg/kg, s.c.) and albuterol (45 mg/kg, s.c.) lowered blood pressure and elevated heart rate to the same extent. Also, both agonists increased the myocardial content of cAMP, decreased the myocardial content of ATP, and elevated serum MB-CPK. The beta1 antagonist practolol, but not the ganglionic blocking agent chlorisondamine, attenuated the elevation in heart rate to albuterol without reducing its effect on blood pressure. Practolol, but not chlorisondamine, abolished the effects of albuterol on cAMP, ATP, and MB-CPK. These data suggest that the myocardial injury which is associated with an increased heart rate and changes in cAMP, ATP, and MB-CPK following the administration of albuterol is not the result of beta2-mediated hypotension, but is due to stimulation of myocardial beta1 receptors.

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