Reduced vascular responsiveness after a single bout of dynamic exercise in the conscious rabbit.
Adenosine/pharmacology; Adrenergic/physiology; Animals; Blood Vessels/*physiology; Dose-Response Relationship; Drug; Hindlimb/physiology; In Vitro Techniques; Isoproterenol/pharmacology; Phenylephrine/pharmacology; Physical Exertion/*physiology; Pressoreceptors/physiology; Purinergic/physiology; Rabbits; Receptors; Reflex/physiology; Regional Blood Flow/physiology
We measured agonist-induced changes in the iliac artery blood flow velocity (IFV) independent of baroreflex-mediated compensatory mechanisms in chronically instrumented New Zealand White rabbits (n = 8). Animals were instrumented with a Doppler flow probe around the right common iliac artery. A Teflon catheter was inserted into the right iliolumbar artery for local infusion of the vasoactive agonists. Another Teflon catheter was inserted in the left femoral artery for the measurement of pulsatile and mean arterial (MAP) blood pressures and heart rate (HR). The alpha-adrenergic receptor agonist phenylephrine (PE, 1.32-10.0 micrograms), the beta 1- and beta 2-adrenergic receptor agonist isoproterenol (IP, 0.022-0.11 micrograms), and the purinergic receptor agonist adenosine (AD, 10.0-100.0 micrograms) were injected into the functionally isolated hindlimb, and dose-response curves were generated. Changes in IFV were obtained without changes in MAP or HR. Exercise increased HR, MAP, and IFV (65.3 +/- 7.1 beats/min, 11.1 +/- 2.2 mmHg, and 2.2 +/- 0.3 kHz, respectively). The maximum responses to PE, AD, and IP were reduced 29.0 +/- 6.7, 50.7 +/- 8.5, and 61.0 +/- 8.1%, respectively, after exercise. In conclusion, exercise attenuated adrenergic and purinergic receptor-mediated vascular responses in the intact conscious rabbit.
Howard M G; DiCarlo S E
Journal of applied physiology (Bethesda, Md. : 1985)
1992
1992-12
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jappl.1992.73.6.2662" target="_blank" rel="noreferrer noopener">10.1152/jappl.1992.73.6.2662</a>
Cholinergic disinhibition in area CA1 of the rat hippocampus is not mediated by receptors located on inhibitory neurons.
2-Amino-5-phosphonovalerate/pharmacology; Action Potentials/drug effects; Adenosine/pharmacology; Animals; Baclofen/pharmacology; Carbachol/pharmacology; Cholinergic/*drug effects; Evoked Potentials/drug effects; GABA-A Receptor Antagonists; Hippocampus/*drug effects; In Vitro Techniques; Membrane Potentials/drug effects; Neurons/*drug effects; Parasympathetic Nervous System/*drug effects; Phorbol Esters/pharmacology; Quinoxalines/pharmacology; Rats; Receptors; Synaptic Transmission/physiology
We studied the effects of carbamylcholine (carbachol; CCh) on monosynaptic inhibitory postsynaptic potentials (IPSPs) evoked in the presence of the excitatory amino acid receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and D,L-2-amino-5-phosphonovalerate (APV). CCh (30 microM) blocked late afterhyperpolarizations but did not depress GABAA receptor-mediated fast monosynaptic IPSPs or GABAB receptor-mediated late monosynaptic IPSPs. In the presence of CCh the GABAB receptor agonist (+/- )-baclofen (2 microM) reversibly hyperpolarized pyramidal neurons and depressed monosynaptic IPSPs as under control conditions. Phorbol-12,13-diacetate (PDAc; 10 microM) increased fast and depressed late monosynaptic IPSPs, and prevented depression of IPSPs by baclofen. These results suggest that cholinergic disinhibition in area CA1 of the hippocampus results from decreased synaptic excitation of inhibitory neurons.
Lambert N A; Teyler T J
European journal of pharmacology
1991
1991-10
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0014-2999(91)90801-v" target="_blank" rel="noreferrer noopener">10.1016/0014-2999(91)90801-v</a>