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B Pernow

Publications and source records attributed to B Pernow.

At least 19 recordsLinked to original sources
PubMed1990

The effect of calcitonin gene-related peptide (CGRP) on human forearm blood flow.

The effect of intravenous and intra-arterially administered calcitonin gene-related peptide (CGRP) on the human forearm blood flow and cutaneous blood flow were investigated by means of venous occlusion plethysmography and laser-Doppler flowmetry, respectively. Infusion of CGRP (11-216 pmol min-1) into the brachial artery resulted in a dose-dependent increase in forearm blood flow and cutaneous blood flow which persisted for up to 90 min after the infusion was stopped. Repeated infusions resulted in an identical response. Systemic intravenous infusion of CGRP (104-520 pmol min-1) resulted in a dose-dependent flush in the face, neck, upper trunck and upper arms, and an increase in the forearm blood flow. The cutaneous blood flow was dramatically increased on the forehead, whereas on the hand only a slight increase was noted. By intravenous infusions a significant drop in blood pressure and increase in heart rate were seen at 520 pmol min-1. Thus, it is possible to give CGRP in doses that increase the blood flow in muscle and skin without resulting in a fall in systemic arterial blood pressure and tachycardia, suggesting that CGRP may be used as a tool for the treatment of various conditions in man with compromised blood flow.

Adolescent↗
PubMed1988

Effects of prostaglandins E2 and F2 alpha on motility of small intestine in man.

Interdigestive motility of the small intestine was examined in 23 fasted healthy volunteers following luminal administration of the prostaglandins E2 and F2 alpha. Motility was monitored by means of water-perfused catheters measuring intraluminal pressure changes. The registration points were located 25 cm apart, in the proximal duodenum, at the angle of Treitz, and in the jejunum. Prostaglandin E2 administered intraduodenally delayed the initiation of the subsequent activity front. The interval to the next activity front was prolonged by a dose of 1.0 mg prostaglandin E2 from 79.5 +/- 9.5 min to 137.1 +/- 5.0 min (P less than 0.01) and to 158.0 +/- 14.0 min by 2.0 mg prostaglandin E2 (P less than 0.05). Also, in four of seven experiments, a progressing activity front was arrested by 2.0 mg prostaglandin E2. Prostaglandin F2 alpha at 2.5 or 5.0 mg given intraduodenally induced bursts of contractions with a frequency of 17.7 +/- 0.8 contractions per minute and an amplitude of 10 to 110 mm Hg (P less than 0.01). In comparison, food intake produced irregular contractions at a frequency of 5.3 +/- 1.8 contractions per minute and an amplitude of 10 to 50 mm Hg (P less than 0.05). It is concluded that prostaglandin E2 delays the initiation of activity fronts in the duodenum. In contrast, prostaglandin F2 alpha changes the interdigestive motility pattern to one of intense contractile activity, which is different from the postprandial motility pattern.

Adult↗
PubMed1986

Plasma neuropeptide Y-like immunoreactivity and catecholamines during various degrees of sympathetic activation in man.

Neuropeptide Y-like immunoreactivity (NPY-LI) and catecholamine concentrations in plasma were analysed during and after 60 min of physical exercise at a work load corresponding to 70% of individual maximal oxygen uptake in nine healthy men of average physical fitness. Systemic plasma NPY-LI increased progressively from 18 +/- 3 to 81 +/- 19 pmol X 1(-1) in parallel with a 10-fold increase in noradrenaline (NA) concentration. The increase in plasma NPY-LI during exercise and the decrease after completion of exercise were much slower than the corresponding changes in NA concentration. This difference is probably related to a slower diffusion of NPY into systemic circulation after release, as well as to a longer half-life of NPY than of NA in plasma. Reversed phase HPLC and sephadex G-50 gel-filtration chromatography revealed that the main component of NPY-LI in plasma during exercise eluted in a similar position as synthetic human NPY. During exercise plasma NPY-LI correlated well with the plasma concentration of NA (r = 0.80), but not with that of adrenaline (ADR), suggesting a neuronal origin of NPY. The self-ratings of perceived exertion (RPE) were well correlated with the plasma concentrations of both NPY-LI and NA. No clear-cut veno-arterial concentration difference was observed for NPY-LI. Isometric handgrip and orthostatic test doubled plasma NA concentrations but did not cause any increase in plasma NPY-LI. No change in plasma tachykinin-like immunoreactivity was detected during exercise. The present data suggest that NPY is released together with NA during strong, but probably not during mild, sympathetic activation under physiological conditions in man.

Adult↗
PubMed1985

Role of tachykinins in neurogenic inflammation.

Recent observations on the distribution, release, and biologic properties of neuropeptides connected to sensory neurons have added new information about the mechanism of hyperemia, plasma extravasation, and increase in smooth muscle tone induced by sensory nerve stimulation and by mechanical, physical, or chemical stimuli. To date, Substance P (SP) is the best characterized of these peptides. Using the skin, eye, and respiratory tract as experimental models, it has been shown that: 1) SP is widely distributed in primary sensory neurons as well as in afferent sensory fibers in the vagus, 2) SP is released from sensory nerve terminals during antidromic stimulation, 3) local administration of SP mimics the effect of sensory nerve stimulation, and 4) hyperemia, plasma leakage, and smooth muscle contractions, normally induced by nerve stimulation or noxious stimuli, are absent in tissues pretreated with the SP depleting agent capsaicin or with SP antagonists. These findings indicate that peptidergic nerve fibers are involved in the local regulation of blood flow, vascular permeability, and the tone of smooth muscles. In addition, they give new insights in the pathophysiology of hyperreactive disorders and neurogenic inflammation.

Animals↗
PubMed1983

Substance P.

Explore the source record for details and available documents.

Analgesics↗
PubMed1982

Distribution of substance P in brain and periphery and its possible role as a co-transmitter.

Substance P is widely distributed in the nervous system. In brain and spinal cord it may act as a transmitter, for example at the central branches of primary sensory neurons. It may also be released from the sensory nerve endings and is thought to be involved in antidromic vasodilatation and in synaptic transmission in autonomic ganglia. In some central neurons substance P is stored together with 5-hydroxytryptamine and thyrotropin-releasing hormone. These neurons project to the ventral horn of the spinal cord, amongst other places. In another system substance P coexists with a cholecystokinin-like peptide. These neurons are localized in the periaqueductal central grey matter and also project to the spinal cord. Finally, injection of a substance P antagonist into the ventral mesencephalon causes marked morphological changes in neurons that contain dopamine, substance P and gamma-aminobutyric acid (GABA).

Animals↗
PubMed1981

Substance P: its distribution, pharmacological actions and possible physiological role in sensory neurons.

The undecapeptide substance P (SP) is a normal constituent of most tissues, particularly the central and peripheral nervous system. SP-immunoreactive cell bodies and terminal networks are distributed in most areas of the brain. Particular interest has been focused on the presence and function of SP in the primary sensory neuron. SP is released from both the central and peripheral part of the sensory neuron following stimulation of the dorsal roots and peripheral sensory nerves. Evidence is given for a transmitter role of SP in the sensory neurons and for the hypothesis that SP is involved in the vascular effects induced by sensory stimulation, referred to as the axon reflex. SP is present in large amounts in the gastro-intestinal tract. By immunohistochemistry SP is demonstrated within nerve cell bodies and terminals of the intramular plexuses but also in extrinsic neurons. It is released both from intrinsic sensory neurons of the gut and from the gastro-intestinal lumen in response to vagal stimulation. SP stimulates motor activity and is ascribed a regulatory role for both the intestinal motility and blood flow. SP has numerous pharmacological effects, the most obvious being excitation of spinal motoneurons, vasodilation and stimulation of salivary and pancreatic secretion. It is a normal constituent of blood plasma but there is no evidence that SP acts as a circulating hormone.

Animals↗
PubMed1980

Cellular localization of peptides in neural structures.

By means of the immunohistochemical technique of Coons and collaborators, numerous peptide-containing neurons have been observed in the brain, spinal cord and periphery. These neurons may contain peptides such as substance P, vasoactive intestinal polypeptide (VIP), enkephalin or somatostatin. Some systems are very extensive. For example, immunoreactive substance P has been observed in more than 30 cell groups in the central nervous system, in primary sensory neurons, in sensory neurons in the vagus nerve and in taste buds, and in intestinal neurons. Thus, one and the same peptide can be utilized at many different levels in the nervous system. Several examples are now known where a regulatory peptide occurs together with a classical transmitter, such as a catecholamine, in the same neuron, which suggests the possibility that a neuron can release more than one transmitter substance. Of particular interest is the occurrence of VIP in presumed cholinergic neurons innervating exocrine glands in the cat, and the coexistence of a cholecystokinin (CCK)-like peptide in dopamine neurons projecting mainly to limbic areas. In the former system VIP seems to be responsible mainly for vasodilation, whereas acetylcholine mainly causes secretion. Furthermore, combined infusion of both substances in very low doses results in a marked potentiation of the secretory and vasodilatory responses. Thus, we have an example where two putative transmitters, released from the same nerve endings, seem to cooperate to activate a physiological response (secretion). With regard to the central CCK/dopamine neurons the type of interaction between the two coexisting transmitter candidates is at present unclear. It is suggested that elucidation of different types of coexistence phenomena may advance our understanding of chemical transmission at synapses under normal and pathological conditions, and may lead to new approaches to the treatment of some nervous disorders.

Adrenocorticotropic Hormone↗