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The most common haemodynamic abnormality in human essential hypertension is an increase in systemic vascular resistance. Morphologic substrate for increased flow resistance is a narrowing of the lumen of arteriolar resistance vessels. During the course of essential hypertension, this is associated with an increase in wall (mainly media) thickness due to hypertrophy and hyperplasia of vascular smooth muscle cells. In contrast to concepts interpreting media thickening strictly as structural adaptation to increased perfusion pressure, various lines of evidence also point to pressure independent factors. In this context, extracellular factors such as 'growth factors' as well as alterations in the activity of intracellular messenger systems must be considered. Recent studies suggest that substances generally known to act as vasoconstrictors such as angiotensin II, noradrenaline and arginine-vasopressin may also stimulate vascular smooth muscle cell growth and proliferation. Intracellular messenger systems with possible significance in the response to trophins and/or mitogens of vascular smooth muscle cells are phospholipase C, protein kinase C and the Na/H-antiport. These systems have been demonstrated to be altered in hypertension supporting the concept that one endogenous factor in human essential hypertension with pathophysiological significance, at least in a subgroup of patients, may be an enhanced reactivity of vascular smooth muscle cells to trophic and mitogenic stimuli. In this context, intracellular messenger systems such as phospholipase C, protein kinase C and/or the Na/H-antiport may play an important pathophysiological role. [ABSTRACT FROM AUTHOR]

In the isolated taenia coli of the guinea-pig, a cooling to 13°C was necessary to suppress the spontaneous activity completely. Under these conditions, regular spikes (intracellular measurements) with contractions can be produced by electrical stimulation. The Ca-content of unstimulated preparations, determined as a basis for fluxmeasurements to test the hypothesis of calcium spikes, was constant during the observation period, 1-3 h after the beginning of the experiment, (3.1 mmole/kg wet weight as compared to 1.9 mmole/kg in the fresh tissue). In the resting state, 63% of the total Ca was exchangeable withCa in 2 h. The exchange could be expressed as the sum of two exponential components with half-times of 0.4 min and 4 min. This allows one to interpret the ion movements, by means of a three compartment model, as transport processes between the organ bath (fraction, S) and the extracellular space (fraction S) as well as between S and a cellular fraction ( S). [ABSTRACT FROM AUTHOR]

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