{'fraction_non_alphanumeric': 0.01823486506199854, 'fraction_numerical': 0.0, 'mean_word_length': 5.471698113207547, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Steady-state autoregulation of renal blood flow: a myogenic model.

This paper presents a model of myogenic control of renal blood flow based on the proposition that steady-state flow occurs when the distending and constricting forces acting on the afferent arteriole are equal. The distending force is represented by the Laplace relationship. The opposing force is governed by the properties of the arterioles and has two components--a purely passive component and an "active" component resulting from vascular smooth muscle contraction. Within the myogenic model, vascular smooth muscle contraction is initiated by "stretch"-induced changes in calcium permeability. Terms are developed describing the effect of stretch on calcium permeability, intracellular calcium, and contractile activity. The model is adapted to describe the myogenic control of blood flow in the dog kidney. Sigmoidal relationships between stretch and calcium permeability and between intracellular calcium and muscle tension seem to account for the shape of the autoregulatory curve. The model predicts a shifting of the autoregulatory pressure-flow curve upward and to the right in response to increased tissue hydrostatic pressure. The model is also exquisitely sensitive to changes in the parameters governing intracellular calcium. These predictions agree well with experimental observations.