SUMMARY1. The release of vasoactive intestinal polypeptide (VIP) into blood from the gastrointestinal tract was studied when eliciting autonomic nervous effects known to be mediated via non-adrenergic, non-cholinergic nerve fibres. All studies were performed on animals given atropine.2. Electrical stimulation of the low threshold vagal fibres to the stomach did not significantly change gastric volume or VIP concentration in the venous effluent from the stomach. Stimulating the high threshold fibres, on the other hand, produced a gastric relaxation concomitant with a significant increase of venous plasma VIP concentration. When eliciting a similar vagal relaxation of the stomach by distending a balloon in the oesophagus a significant increase of venous plasma VIP concentration was also recorded.3. Mechanical stimulation of the mucosa of the small bowel increased intestinal blood flow and a significant increase of venous plasma VIP concentration was observed.4. Stimulation of the pelvic nerves to the colon produced a transient vasodilation and a significant increase of VIP in the venous effluent from the large bowel. A maintained vasodilation in the colon was induced by mechanically stimulating the rectal mucosa. This vascular response was accompanied by a significant raise of venous plasma VIP concentration.5. The results demonstrate that all the studied nervous effects known to be mediated via non-adrenergic, non-cholinergic nerve fibres were accompanied by significant increases of the VIP concentration in the venous effluent. The possible physiological implications of these findings are discussed and it is proposed that VIP may be a neurotransmitter in the gastrointestinal tract.
Progressive central hypovolemia is characterized by a normotensive, tachycardic stage followed by a reversible, hypotensive stage with slowing of the heart rate (HR). We investigated circulatory changes and arterial hormone concentrations in response to lower-body negative pressure (LBNP) in six volunteers before and after atropine administration. LBNP of 55 mmHg initially resulted in an increase in HR from 55 +/- 4 to 90 +/- 5 beats/min and decreases in mean arterial pressure (MAP) from 94 +/- 4 to 81 +/- 5 mmHg, in central venous pressure from 7 +/- 1 to -3 +/- 1 mmHg, and in cardiac output from 6.1 +/- 0.5 to 3.7 +/- 0.11/min. Concomitantly, epinephrine and norepinephrine levels increased. After 8.2 +/- 2.3 min of LBNP, the MAP had decreased to 41 +/- 7 mmHg and HR had decreased to 57 +/- 3 beats/min. Vasopressin increased from 1.2 +/- 0.3 to 137 +/- 45 pg/ml and renin activity increased from 1.45 +/- 4.0 to 3.80 +/- 1.0 ng.ml-1.h-1 with no further changes in epinephrine, norepinephrine, and vasoactive intestinal polypeptide. A tardy rise in pancreatic polypeptide indicated increased vagal activity. After atropine. LBNP also caused an initial increase in HR, which, however, remained elevated during the subsequent decrease in MAP to 45 +/- 6 mmHg occurring after 8.1 +/- 2.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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