Different patterns of respiratory and cardiovascular responses elicited by chemical stimulation of dorsal medulla in the rat

2000 ◽  
Vol 857 (1-2) ◽  
pp. 99-109 ◽  
Author(s):  
V. Marchenko ◽  
H.N. Sapru
Keyword(s):  
Cardiovascular Responses ◽  
Chemical Stimulation ◽  
Dorsal Medulla ◽  
Stimulation Of

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.

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.

Coactivation of renal sympathetic neurons and somatic motor neurons by chemical stimulation of the midbrain ventral tegmental area

2011 ◽  
Vol 110 (5) ◽  
pp. 1342-1353 ◽  
Author(s):  
Tomoko Nakamoto ◽  
Kanji Matsukawa ◽  
Nan Liang ◽  
Rie Wakasugi ◽  
L. Britt Wilson ◽  
...  
Keyword(s):  
Ventral Tegmental Area ◽  
Sympathetic Nerve ◽  
Cardiovascular Responses ◽  
Chemical Stimulation ◽  
Homocysteic Acid ◽  
Renal Sympathetic Nerve ◽  
Anesthetized Rats ◽  
Ventral Tegmental ◽  
Renal Sympathetic ◽  
Stimulation Of

We examined whether neurons in the midbrain ventral tegmental area (VTA) play a role in generating central command responsible for autonomic control of the cardiovascular system in anesthetized rats and unanesthetized, decerebrated rats with muscle paralysis. Small volumes (60 nl) of an N-methyl-d-aspartate receptor agonist (l-homocysteic acid) and a GABAergic receptor antagonist (bicuculline) were injected into the VTA and substantia nigra (SN). In anesthetized rats, l-homocysteic acid into the VTA induced short-lasting increases in renal sympathetic nerve activity (RSNA; 66 ± 21%), mean arterial pressure (MAP; 5 ± 2 mmHg), and heart rate (HR; 7 ± 2 beats/min), whereas bicuculline into the VTA produced long-lasting increases in RSNA (130 ± 45%), MAP (26 ± 2 mmHg), and HR (66 ± 6 beats/min). Bicuculline into the VTA increased blood flow and vascular conductance of the hindlimb triceps surae muscle, suggesting skeletal muscle vasodilatation. However, neither drug injected into the SN affected all variables. Renal sympathetic nerve and cardiovascular responses to chemical stimulation of the VTA were not essentially affected by decerebration at the premammillary-precollicular level, indicating that the ascending projection to the forebrain from the VTA was not responsible for evoking the sympathetic and cardiovascular responses. Furthermore, bicuculline into the VTA in decerebrate rats produced long-lasting rhythmic bursts of RSNA and tibial motor nerve discharge, which occurred in good synchrony. It is likely that the activation of neurons in the VTA is capable of eliciting synchronized stimulation of the renal sympathetic and tibial motor nerves without any muscular feedback signal.

Baroreceptor activation or glutamate coinjection facilitates depressor responses to ANF microinjection into NTS

1989 ◽  
Vol 257 (2) ◽  
pp. R405-R409
Author(s):  
D. J. McKitrick ◽  
F. R. Calaresu
Keyword(s):  
Electrical Stimulation ◽  
Significant Interaction ◽  
Cardiovascular Responses ◽  
Solitary Tract ◽  
Aortic Depressor Nerve ◽  
Male Wistar Rats ◽  
Threshold Doses ◽  
Baroreceptor Activation ◽  
Dorsal Medulla ◽  
Stimulation Of

As microinjection of atrial natriuretic factor (ANF) into the nucleus of the solitary tract (NTS) has been shown to elicit depressor responses [D. J. McKitrick and F. R. Calaresu. Am. J. Physiol. 255 (Regulatory Integrative Comp. Physiol. 24): R182-R187, 1988], we investigated the possibility that these responses might be facilitated either by electrical stimulation of arterial baroreceptor fibers in the aortic depressor nerve (ADN) or by simultaneous microinjection of L-glutamate (Glu) into the same sites in the NTS. Male Wistar rats (n = 51) were anesthetized with urethan (1.4 g/kg ip), artificially ventilated, and the dorsal medulla was exposed. The ADN was isolated, cut distally, and the central end was placed on bipolar stimulating electrodes. Threshold doses of 10(-7) M ANF microinjected into the NTS were combined with threshold electrical stimulation of the ADN (n = 37) or threshold doses of 0.13-0.5 M Glu (n = 14) microinjected into the NTS. There was a significant interaction between ANF microinjection and ADN stimulation in producing changes in mean arterial pressure (MAP) and heart rate [HR; P less than 0.05; -20.2 +/- 2.3 (SE) mmHg and -30.8 +/- 6.9 (SE) beats/min, respectively; n = 18]. There was also a significant interaction between ANF and Glu in producing changes in MAP and HR [P less than 0.05; -16.3 +/- 1.8 (SE) mmHg and -15.0 +/- 3.0 (SE) beats/min, respectively; n = 8]. These results indicate that ANF influences neurons in the NTS, which are also influenced by activation of arterial baroreceptors, and ANF and Glu interact in the NTS to produce facilitated cardiovascular responses.

Cardiovascular responses to chemical and electrical stimulation of amygdala in rats

1987 ◽  
Vol 253 (5) ◽  
pp. R712-R718 ◽  
Author(s):  
A. J. Gelsema ◽  
D. J. McKitrick ◽  
F. R. Calaresu
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Neuronal Cell ◽  
Cardiovascular Responses ◽  
Chemical Stimulation ◽  
Anatomic Site ◽  
Neuronal Cell Bodies ◽  
Cardiovascular Variables ◽  
Amygdaloid Nuclei ◽  
Stimulation Of

Electrical stimulation of the amygdala has been shown to produce changes in cardiovascular variables. To locate neuronal cell bodies responsible for these changes, responses of arterial pressure (AP) and heart rate (HR) to DL-homocysteate (DLH, 0.15 M, 50-100 nl) microinjected into sites in three amygdaloid nuclei were compared with responses to electrical (90-150 microA) stimulation of the same sites in 35 artificially ventilated, paralyzed, urethan-anesthetized rats. Electrical stimulation resulted in depressor responses in most sites (89%). Changes in AP were accompanied by variable changes in HR. Chemical stimulation produced significantly fewer (25%) depressor responses. Similar results were obtained with injections of 1.0 M DLH. To eliminate the influence of the anesthetic on these responses, AP was recorded in nine conscious rats while stimulating the amygdala. Changes in behavior and AP in these animals could be obtained only by electrical stimulation. These results may be interpreted to indicate either that cell bodies responsible for changes in cardiovascular variables during electrical stimulation are not located in the amygdala or that chemical and electrical stimulation affect different neuronal elements in circuits located in the same anatomic site.

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