Role of spinal NK1 receptors in cardiovascular responses to chemical stimulation of the gallbladder

1995 ◽  
Vol 268 (2) ◽  
pp. H526-H534 ◽  
Author(s):  
H. L. Pan ◽  
A. C. Bonham ◽  
J. C. Longhurst
Keyword(s):  
Intrathecal Injection ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Pressure Change ◽  
Left Ventricular ◽  
Chemical Stimulation ◽  
Intrathecal Catheter ◽  
Nk1 Receptors ◽  
Stimulation Of

The present study examined the role of substance P (SP) as a sensory neurotransmitter in cardiovascular responses to bradykinin applied on the gallbladder. Experiments were performed in anesthetized cats in which sympathetic chains were transected at the T5-T6 level, and the tip of the intrathecal catheter was positioned at T6-T7 to limit the injectate between T6 and L2. Bradykinin (10 micrograms/ml) was applied onto the gallbladder before and after intrathecal injection of [D-Pro2,D-Phe7,D-Trp9]SP (100–200 micrograms, NK1/NK2-receptor antagonist), CP-99,994 (50–100 micrograms, selective NK1 antagonist), MEN-10,376 (100–500 micrograms, selective NK2 antagonist), or vehicle. Intrathecal injection of NK1 but not NK2 antagonist significantly reduced increases in mean arterial pressure, heart rate, and maximal rate of left ventricular pressure change by 28 +/- 2 mmHg (33 +/- 4%), 4 +/- 1 beats/min (42 +/- 5%), and 497 +/- 46 mmHg/s (36 +/- 4%), respectively. Intrathecal injection of NK1 or NK1/NK2 antagonist had no effect on cardiovascular responses evoked by electrical stimulation in the rostral ventral lateral medulla. These data suggest that endogenous SP, acting as a sensory neurotransmitter, is involved in the excitatory cardiovascular reflex caused by chemical stimulation of the gallbladder through its action on NK1 receptors in the spinal cord.

Stimulation of pancreatic afferents reflexly activates the cardiovascular system in cats

1983 ◽  
Vol 245 (6) ◽  
pp. R820-R826 ◽  
Author(s):  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell
Keyword(s):  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Chemical Stimulation ◽  
Potential Mechanism ◽  
Bilateral Vagotomy ◽  
Reflex Activation ◽  
Developed Pressure ◽  
Stimulation Of

Chemical stimulation of afferents from the stomach and gallbladder has been shown reflexly to activate the cardiovascular system. It is not known, however, whether stimulating afferents from the pancreas evoke similar reflex activity. Therefore we recorded the cardiovascular responses in cats anesthetized with methoxyflurane, while we applied capsaicin (200 micrograms/ml) and bradykinin (0.001-1,000 micrograms/ml) to the surface of the pancreas. Topically applying these algesic substances evoked cardiovascular responses that included increases in systemic arterial pressure, heart rate, left ventricular dP/dt at 40-mmHg developed pressure and systemic vascular resistance. Bilateral vagotomy at the level of the diaphragm did not diminish the cardiovascular responses evoked by capsaicin or bradykinin. In contrast, removal of the celiac and superior mesenteric ganglia abolished the cardiovascular responses demonstrated previously when capsaicin or bradykinin was applied to the pancreas. We conclude that afferent endings in the pancreas can be stimulated reflexly to increase cardiovascular function in cats. This reflex activation represents a potential mechanism for eliciting the cardiovascular changes observed during acute pancreatitis, particularly the marked vasoconstriction that may lead to renal failure.

Similarity of cardiovascular responses to exercise and to diencephalic stimulation

1960 ◽  
Vol 198 (6) ◽  
pp. 1139-1142 ◽  
Author(s):  
Orville A. Smith ◽  
Robert F. Rushmer ◽  
Earl P. Lasher
Keyword(s):  
Heart Rate ◽  
Third Ventricle ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
The Third ◽  
Stimulating Electrodes ◽  
Stimulation Of

Devices to measure left ventricular pressure, diameter and heart rate in animals with closed chests were placed on the hearts of dogs. After recovery from this operation the dogs were trained to exercise on a treadmill and the cardiovascular responses to this exercise were recorded. Stimulating electrodes were then stereotaxically placed in the diencephalon. In some dogs the electrodes were chronically implanted, and the stimulation was carried out after recovery from this second operation. In other animals stimulation was carried out immediately while they were under chloralose anesthesia. Stimulation of the H1 and H2 fields of Forel and the periventricular gray of the third ventricle resulted in cardiovascular responses similar to those which result from exercise.

Cardiac cyclic nucleotides and norepinephrine during neural sympathetic stimulation

1981 ◽  
Vol 240 (4) ◽  
pp. H630-H635
Author(s):  
M. T. Pindok ◽  
E. Sukowski ◽  
V. V. Glaviano
Keyword(s):  
Cyclic Nucleotides ◽  
Pressure Rise ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Muscarinic Agonist ◽  
Sympathetic Stimulation ◽  
Cardiac Responses ◽  
Stimulation Period ◽  
Stimulation Of

The role of the cardiac cyclic nucleotides, adenosine 3',5'-monophosphate (cAMP) and guanosine 3',5'-monophosphate (cGMP), and norepinephrine (NE) in cardiac responses to stimulation of the left ansa subclavia were studied in anesthetized open-chest dogs. In three groups of dogs undergoing stimulation for 6 min with impulse frequencies of 4, 10, or 20 Hz and 5 V, left ventricular levels of cAMP, cGMP, and NE were determined at the end of the stimulation period and compared to control dogs. A significant elevation in cAMP (avg 67%) was found at all three frequencies. Myocardial NE decreased by an average of 58% from control by the end of the stimulation period, regardless of the stimulation frequency. The rate of left ventricular pressure rise (LV dP/dt) was found to be linearly related to the increase in myocardial cAMP (P less than 0.01) rather than to NE levels found after stimulation. Propranolol administered before ansa subclavia stimulation caused significant decreases in both cAMP and LV dP/dt, whereas the muscarinic agonist carbachol, caused increases in cGMP and NE and a decrease in LV dP/dt accompanied by a nonsignificant decline in cAMP. The elevation in levels of cGMP and NE and the decrease in LV dP/dt to carbachol were blocked with atropine. Results from pretreating dogs with propranolol and carbachol followed by neural sympathetic stimulation indicated the importance of beta-adrenergic and muscarinic receptors in modifying cardiac function through the production of the cyclic nucleotides. Sustained cardiac responses during ansa subclavia stimulation at physiological levels could be related to the accelerated synthesis of endogenous cAMP.

A Sympathetic Hypertensive Reflex from the Heart of Conscious Dogs

1981 ◽  
Vol 61 (s7) ◽  
pp. 181s-183s ◽  
Author(s):  
M. Pagani ◽  
P. Pizzinelli ◽  
R. Furlan ◽  
S. Guzzetti ◽  
O. Rimoldi ◽  
...  
Keyword(s):  
Sensory Nerve ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Chemical Stimulation ◽  
Vagal Afferents ◽  
Sensory Innervation ◽  
Conscious Dogs ◽  
Sympathetic Reflexes ◽  
Depressor Reflex ◽  
Stimulation Of

1. The aim of the present experiments was to study in conscious animals the effect of chemical stimulation of cardiac sensory innervation by bradykinin, a physiological substance known to activate both vagal and sympathetic cardiac sensory nerve endings, at doses devoid of systemic haemodynamic effects. 2. In conscious dogs with implanted catheters bradykinin (100 ng/kg) injected into a cannulated branch of the left coronary artery induced significant (P < 0.01, n = 5) reflex increases in mean arterial pressure and heart rate as well as increases in left ventricular pressure, left ventricular dP/dt max. and coronary blood flow. 3. These changes were obtained in the absence of pain reactions. 4. The concept, derived from experiments on anaesthetized animals, that chemical stimulation of the intact sensory supply of the heart always elicits a cardiovascular depressor reflex mediated by cardiac vagal afferents has to be modified, as pressor sympathetic reflexes may occur after an appropriate stimulus to the fully innervated heart of conscious dogs.

Role of paraventricular and supraoptic nuclei in central cardiovascular regulation in the cat

1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Cardiovascular Responses ◽  
Inhibitory Influence ◽  
Sympathetic Nervous Systems ◽  
Aortic Depressor Nerve ◽  
Bilateral Lesions ◽  
Alpha Chloralose ◽  
Supraoptic Nuclei ◽  
Stimulation Of

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.

Effects of intravenous anesthetic agents on left ventricular function in dogs

1977 ◽  
Vol 232 (1) ◽  
pp. H44-H48
Author(s):  
L. D. Horwitz
Keyword(s):  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Intravenous Anesthetic ◽  
First Derivative ◽  
Anesthetic Agents ◽  
Thiopental Sodium ◽  
Stimulation Of ◽  
Mean Heart Rate

The cardiovascular effects of ketamine hydrochloride and thiopental sodium were studied in 11 dogs. During anesthesia, mean heart rate rose to 185 beats/min with ketamine and 147 beats/min with thiopental. Cardiac output was increased with ketamine but unchanged by thiopental. The maximum first derivative of the left ventricular pressure (dP/dt max) fell by 14% with thiopental but did not change significantly with ketamine. Propranolol resulted in attenuation of the tachycardia and a fall of 10% in dP/dt max with ketamine but had little effect on the response to thiopental. Phentolamine had no consistent effects on either drug. With pentolinium both drugs decreased dP/dt max. Intracoronary injection of ketamine decreased dP/dt max. Adrenalectomy had little effect on the responses to either anesthetic. The results lead to the conclusion that both ketamine and thiopental have myocardial depressant effects, but, whereas thiopental does not alter sympathetic tone, the depressive effects of ketamine are obscured by stimulation of cardiac sympathetic nerves.

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Hemodynamic Changes ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

Effects of alpha-adrenergic blockade on cardiovascular responses to static exercise in cats

1986 ◽  
Vol 250 (1) ◽  
pp. R1-R4
Author(s):  
T. G. Waldrop ◽  
M. Bielecki ◽  
W. J. Gonyea ◽  
J. H. Mitchell
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Static Exercise ◽  
Ventricular Systolic Pressure ◽  
Pressure Transducers ◽  
Adrenergic Mechanism ◽  
Alpha Blockade

Static exercise performed by conscious cats elicits increases in heart rate (HR), left ventricular systolic pressure (LVSP), and the maximal rate of left ventricular pressure development [LV(dP/dt)max]. The increased HR is mediated primarily by withdrawal of parasympathetic tone, whereas a beta-adrenergic mechanism is responsible for the LV(dP/dt)max increase. In the present study the cardiovascular responses to static exercise in awake cats was recorded before and after alpha-adrenergic blockade. Pressure transducers were implanted into the left ventricle of cats who had been trained operantly to perform static exercise. Significant increases in LVSP, LV(dP/dt)max and HR occurred in all cats during static exercise before blockade. In contrast, alpha-adrenergic blockade (phentolamine, 2.5 mg/kg iv) abolished the exercise-induced increase in LVSP but did not prevent increases in HR and LV(dP/dt)max. The cats performed fewer exercise bouts per day during alpha-blockade than when unblocked. We conclude that an alpha-adrenergic mechanism mediates the increase in LVSP in response to static exercise in conscious cats.

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