TY - JOUR
T1 - Carviobascular alterations associated with bursts of panting in the exercising dog
AU - Dampney, R. A. L.
PY - 1974/4/1
Y1 - 1974/4/1
N2 - 1. In conscious dogs exercising on a treadmill variations in arterial blood pressure and heart rate which were correlated with bursts of panting were observed. The blood pressure variations reflected similar variations in the total peripheral vascular resistance. 2. During exercise a change in respiration from slow breathing to panting was followed by a systemic vasodilatation and fall in blood pressure, but a rise in heart rate. Analysis of the time course of these effects demonstrated that the heart rate increase occurred later than the blood pressure fall. 3. The correlation between panting and blood pressure changes was not abolished by either of the receptor‐blocking drugs atropine sulphate or propranolol, nor by either of the following surgical procedures: acute bilateral cervical vagotomy, and denervation of the carotid sinus baroreceptors and carotid body chemoreceptors. 4. The vasodilatation which followed a burst of panting appeared to be due to a decrease in adrenergic vasoconstrictor sympathetic nerve activity, and not to a change in the chemical composition of the arterial blood. 5. It is concluded that the vascular changes are not reflex responses to stimulation of peripheral receptors by the bursts of panting. Instead, it is suggested that both the bursts of panting and associated falls in blood pressure are parallel effects resulting from activation at a suprabulbar level of the central nervous system. It is also concluded that the variations in heart rate are mediated by the baroreceptor reflex mechanism, activated by the changes in mean blood pressure.
AB - 1. In conscious dogs exercising on a treadmill variations in arterial blood pressure and heart rate which were correlated with bursts of panting were observed. The blood pressure variations reflected similar variations in the total peripheral vascular resistance. 2. During exercise a change in respiration from slow breathing to panting was followed by a systemic vasodilatation and fall in blood pressure, but a rise in heart rate. Analysis of the time course of these effects demonstrated that the heart rate increase occurred later than the blood pressure fall. 3. The correlation between panting and blood pressure changes was not abolished by either of the receptor‐blocking drugs atropine sulphate or propranolol, nor by either of the following surgical procedures: acute bilateral cervical vagotomy, and denervation of the carotid sinus baroreceptors and carotid body chemoreceptors. 4. The vasodilatation which followed a burst of panting appeared to be due to a decrease in adrenergic vasoconstrictor sympathetic nerve activity, and not to a change in the chemical composition of the arterial blood. 5. It is concluded that the vascular changes are not reflex responses to stimulation of peripheral receptors by the bursts of panting. Instead, it is suggested that both the bursts of panting and associated falls in blood pressure are parallel effects resulting from activation at a suprabulbar level of the central nervous system. It is also concluded that the variations in heart rate are mediated by the baroreceptor reflex mechanism, activated by the changes in mean blood pressure.
UR - http://www.scopus.com/inward/record.url?scp=0016379648&partnerID=8YFLogxK
U2 - 10.1113/jphysiol.1974.sp010508
DO - 10.1113/jphysiol.1974.sp010508
M3 - Article
C2 - 4838797
AN - SCOPUS:0016379648
SN - 0022-3751
VL - 238
SP - 17
EP - 36
JO - Journal of Physiology
JF - Journal of Physiology
IS - 1
ER -