Effects of cold, eating, efferent nerve stimulation and angiotensin on heart rate in sheep before and after autonomic blockade

Hays, F. L.; Webster, A. J. F.

doi:10.1113/jphysiol.1971.sp009507

Cited by 19 publications

(8 citation statements)

References 19 publications

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“…The increase in HR of the cat during eating was reduced by propranolol, which is similar to previous reports on the dog (VATNER et al, 1970a;HAYS and WEBSTER, 1971). The effect of propranolol on the HR response to eating suggested that the acceleration of HR may be evoked at least partially by an increase in sympathetic nerve activity.…”

Section: Discussionsupporting

confidence: 90%

Transient responses of heart rate, arterial pressure, and head movement at the beginning of eating in awake cats.

Matsukawa¹,

Ninomiya²

1985

Jpn.J.Physiol

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Time courses of heart rate (HR), arterial pressure (AP), and head movement at the beginning of eating were analyzed in conscious cats. The cats were trained to eat when movements of their body trunks were restrained. Food was presented for 10 sec at intervals of 100 sec. With the abrupt presentation of food, a head-down movement occurred immediately and thereafter eating started with a mean latency of 1.6 sec. During eating HR increased by 22% from the preeating value and AP was elevated by 11 %. To determine the time relation between the onset of eating and the change in each variable in response to eating, mean time courses of HR, AP, and head movement were obtained from 7-40 trials in each cat. The head-down movement preceded the onset of eating by 1.3 sec. The increase in HR preceded the onset of eating by 0.2 sec; the change in AP followed it by 3-4 sec. This indicated that the increase in HR was not induced reflexly either by food intake or by the change in AP. After administration of hexamethonium, the changes in HR and AP in response to eating were abolished, although eating was evoked by the food presentation. Additionally, the increase in HR was also reduced by propranolol and atropine. Thus, the acceleration of HR at the beginning of eating may be induced by central activation of the autonomic nervous system.

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Section: Discussionsupporting

confidence: 90%

Transient responses of heart rate, arterial pressure, and head movement at the beginning of eating in awake cats.

Matsukawa¹,

Ninomiya²

1985

Jpn.J.Physiol

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“…The present experiments show that this is the case and thus provide further support for the hypothesis of Hays & Webster (1971) that angiotensin is directly responsible for some of the changes in cardiac function observed during eating in the sheep.…”

Section: Discussionsupporting

confidence: 74%

“…Hays & Webster (1971) suggested that the tachycardia accompanying eating in sheep might be due to a direct cardioaccelerator action of angiotensin, since plasma angiotensin levels are elevated during eating (BlairWest & Brook, 1969) and angiotensin was shown to have a cardioaccelerator effect after surgical and pharmacological inhibition of autonomic influences on the heart of anaesthetized sheep (Hays & Webster, 1971).…”

Section: Discussionmentioning

confidence: 99%

Changes during eating in oxygen consumption, cardiac function and body fluids of sheep

Christopherson¹,

Webster²

1972

The Journal of Physiology

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3. Arterial Po. did not change significantly during eating. However PV 02 fell slightly but significantly. The 02 saturation of venous blood fell due to the decline in pH. Estimated CO2 in arterial blood increased as a consequence of increased haemoglobin content. The net effect was to increase arteriovenous difference in 02 content from 4-4 ml./100 ml. before eating to 6-0 ml./100 ml. at the end of the meal.4. 02 consumption increased about 60 % during eating and fell rapidly thereafter. Heart rate followed a similar pattern. Cardiac output however increased only about 17 %, from 6 to 7 1./min. Consequently stroke volume declined throughout the meal from 76 to 52 ml./beat.5. Plasma volume, estimated from measurements of T-1824, declined sharply by about 300 ml. at the beginning of the meal and recovered slowly after feed was removed. Blood volume declined less because of a rise in circulating erythrocytes.6. Extracellular fluid volume was estimated from measurements of thiocyanate and thiosulphate spaces. Thiocyanate space measurements were abandoned after thiocyanate was found to be concentrated in saliva.Considerable random variation occurred in measurements of changes in extracellular fluid from thiosulphate disappearance but the results did

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“…However, it should be noted that vagal withdrawal is likely to induce only a modest rise in heart rate in sheep. Previous studies both from our laboratory (unpublished data) and from the literature (Hays & Webster 1971, Lumbers & Yu 1999 show that i.v. atropine or vagal section increases heart rate in sheep by w20-30 bpm with the maximum heart rates observed following withdrawal of vagal tone being 110-120 bpm.…”

Section: Discussionmentioning

confidence: 95%

Urocortin 2 induces potent long-lasting inhibition of cardiac sympathetic drive despite baroreflex activation in conscious sheep

Charles

Jardine²,

Rademaker³

et al. 2009

Journal of Endocrinology

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Emerging evidence suggests that the urocortin (UCN) peptides contribute to pressure and volume regulation with possible involvement in the pathophysiology of cardiovascular disease. We have recently reported that i.v. UCN1 potently inhibits cardiac sympathetic nerve activity (CSNA) in normal sheep. However, little is known about possible interactions between UCN2 and the sympathetic nervous system. Accordingly, we have examined the effects of i.v. UCN2 on CSNA, hemodynamics, and plasma catecholamines in normal conscious sheep. Bolus i.v. administration of UCN2 (25 and 100 mg) resulted in the expected hemodynamic actions including transient falls in arterial pressure (PZ0 . 016) and more sustained rises in heart rate (P!0 . 001) and cardiac output (P!0 . 001) and falls in peripheral resistance (P!0 . 001). CSNA burst frequency showed a biphasic response (P!0 . 001) with an acute rise followed by a more prolonged fall. CSNA burst area and incidence showed prolonged, dose-dependent falls in response to UCN2 administration (all P!0 . 001). UCN2 also induced a short-lived rise in plasma norepinephrine levels (PZ0 . 006).The marked rise in heart rate in response to UCN2 is preserved in sheep undergoing pharmacological ganglionic blockade with hexamethonium. In conclusion, this is the first study to report the effects of UCN2 on SNA and indicates potent inhibition of sympathetic traffic to the heart despite a generalized baroreceptor-induced activation of sympathetic activity. These findings suggest an important role for UCN2 in cardiovascular homeostasis and warrant further investigation for potential therapeutic applications in acute myocardial injury and heart disease.

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Effects of cold, eating, efferent nerve stimulation and angiotensin on heart rate in sheep before and after autonomic blockade

Cited by 19 publications

References 19 publications

Transient responses of heart rate, arterial pressure, and head movement at the beginning of eating in awake cats.

Transient responses of heart rate, arterial pressure, and head movement at the beginning of eating in awake cats.

Changes during eating in oxygen consumption, cardiac function and body fluids of sheep

Urocortin 2 induces potent long-lasting inhibition of cardiac sympathetic drive despite baroreflex activation in conscious sheep

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