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Biomedical subjects

S I Said

Publications and source records attributed to S I Said.

225 records · Page 13Linked to original sources
PubMedDate not supplied

Evidence that vasoactive intestinal polypeptide is a dilator transmitter to some cerebral and extracerebral cranial arteries.

Many arteries of the head upon electrical stimulation of the non-adrenergic nerve terminals present in their wall exhibit dilation that is only partially reduced by atropine. The results of three types of experiments are presented that tend to implicate vasoactive intestinal polypeptide (VIP) a known vasodilator, as an atropine-resistant dilator transmitter. VIP activity is high in vessels that exhibit neurogenic dilation and low in those that do not. It is released from two arteries that show such dilation upon neurogenic field stimulation and VIP antiserum reduces neurogenic dilation. It is proposed that VIP as well as acetylcholine are released from the innervation of some cranial arteries and together in a number of animals of least are responsible for part of the complex neurogenic dilation witnessed in these vessels. Although substance P is present in nerves found within the wall of cerebral and other cranial blood vessels, it is either ineffective as a dilator in vessels that show a sizeable dilation to electrical stimulation, or else exhibits marked, rapid, persistent tachyphylaxis.

Acetylcholine↗
PubMedDate not supplied

Vasoactive intestinal peptide evokes endothelium-dependent relaxation and cyclic AMP accumulation in rat aorta.

We have investigated VIP-induced relaxation and cyclic AMP accumulation in rat thoracic aorta strips, and the importance of endothelium to both actions. The relaxation was greatly attenuated by removal of endothelium, but was unaltered by cyclo-oxygenase or lipoxygenase inhibitors. Similarly, cyclic AMP formation was nearly abolished with loss of endothelium, but was largely unaffected by inhibitors of arachidonate pathways, cytochrome P450 or guanylate cyclase. VIP may stimulate the release of a diffusible factor from endothelium (an EDRF), which activates adenylate cyclase and relaxes aortic smooth muscle.

Animals↗
PubMedDate not supplied

Characterization of VIP- and helodermin-preferring receptors on human small cell lung carcinoma cell lines.

We investigated the molecular and pharmacologic characteristics of VIP receptors on two human SCLC cell lines: NCI-N592 and NCI-H345. With NCI-N592 cell, the order of potency of VIP-related peptides in inhibiting 125I-VIP binding and in stimulating cAMP production was typical of the human VIP receptor. By covalent cross-linking, a polypeptide of Mr 62,300 was obtained. Conversely, the behavior of NCI-H345 cell line was totally different: helodermin was the most potent peptide, VIP and PHI were equipotent, while hGRF and secretin were totally ineffective. These results suggest that NCI-N592 cells possess a typical VIP receptor while NCI-H345 cells possess a helodermin-preferring receptor, and that the natural target of helodermin might not be the VIP receptor.

Carcinoma, Small Cell↗
PubMedDate not supplied

Inotropic responsiveness in hypertensive left ventricular hypertrophy: impaired inotropic response to glucagon and vasoactive intestinal peptide in renal hypertensive rats.

Previous studies have shown that left ventricular (LV) hypertrophy in renal hypertensive rats (RHR) is associated with reduced responsiveness to beta-adrenergic stimulation (isoproterenol) but not to calcium or cardiac glycosides. To determine whether this impairment is restricted to beta-receptor agonists or extended to include other stimulants of the adenylate cyclase system, inotropic responses to glucagon and to vasoactive intestinal peptide (VIP) were determined in isolated paced hearts (Langendorff preparation) from RHR and strictly matched sham-operated controls. The response (delta peak LV +dP/dt) to both agonists was significantly reduced in RHR, whether expressed in absolute value or in percent of baseline. It averaged 59.3 +/- 19.3 (SE) mm Hg X s-1 in RHR at the highest dose of VIP (15 micrograms) and a perfusion pressure (PP) of 50 mm Hg as compared with 255 +/- 68.4 in controls (p less than 0.01). The responses to glucagon were determined at two levels of perfusion pressure--50 and 80 mm Hg--to determine the influence, if any, of possible alterations in myocardial perfusion on differences between the normal and hypertrophied hearts. At both PP levels the LV +dP/dt response was significantly lower in RHR--+ 374 +/- 103 vs. + 1,026 +/- 166 mm Hg X s-1 (p less than 0.005) or + 120 +/- 5 vs. + 143 +/- 7% of baseline value (p less than 0.02) for PP of 50 mm Hg; and 392 +/- 154 vs. + 1,732 +/- 251 mm Hg X s-1 (p less than 0.01) or + 112 +/- 4 vs. + 160 +/- 2% (p less than 0.001) for PP of 80 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Vasoactive peptides. State-of-the-art review.

At least 16 naturally occurring peptides either constrict or dilate blood vessels. Many of these peptides are present in nerve cells and nerve terminals supplying systemic and pulmonary blood vessels and the heart. Such neuropeptides are released locally as neurotransmitters, and can influence vascular tone, local and regional blood flow, arterial blood pressure, and cardiac function. There is evidence for the participation of at least some vasoactive peptides in the regulation of these functions and in the mediation or modulation of systemic shock and arterial hypertension. The investigation of vasoactive peptides in relation to cardiovascular function and dysfunction is at a promising threshold.

Angiotensin II↗
PubMedDate not supplied

Novel peptides in the lung.

Peptides found in the normal lung are described, and present theories as to their functions are presented.

Angiotensin II↗
PubMedDate not supplied

Platelet-activating factor increases pulmonary microvascular permeability and induces pulmonary edema. A preliminary report.

Platelet-activating factor, a naturally occurring lipid that is released from leukocytes and alveolar macrophages, increased the flow of protein-rich lymph from the lungs and induced pulmonary edema in dogs when given in picomolar doses. The pulmonary edema was due to increased microvascular permeability, probably secondary to endothelial cell injury. These observations suggest that platelet-activating factor may be a mediator of high-permeability pulmonary edema in the "respiratory distress syndrome" complicating acute lung injury.

Animals↗