Salt, obesity, and alcohol fail to induce a lasting rise of blood pressure with age, and may be independent of renocortical vasculopathy

QJM. 1999 Oct;92(10):601-7. doi: 10.1093/qjmed/92.10.601.

Abstract

Essential hypertension has a multitude of aetiologies, environmental circumstances that impact harmfully upon blood pressure levels. These aetiologies fall into two types: a reversible type that requires continuous exposure to the inciting agent to sustain the elevated blood pressure, and a persistent type which introduces some form of permanent change, presumably in body tissues. Available data on salt overload, obesity, and alcohol tend to cast these agents as reversible, without persistent effects. Agents of the reversible type emerge here as unlikely candidates for explaining the rise of blood pressure with age. Evidence reviewed here implicates intimal fibroplasia in renocortical arteries as the accumulated record that causes rising of blood pressure with age by Goldblatt mechanisms actuated through nephron heterogeneity. Such mechanisms could explain the persistent effects that propel the rise of blood pressure with age at varying rates among world-wide populations. These findings offer a new starting place for efforts to discover the aetiological agents that propel the rise of blood pressure with age, agents that apparently do not include salt, obesity, or alcohol.

Publication types

  • Review

MeSH terms

  • Adult
  • Aged
  • Aging / physiology*
  • Alcohol Drinking / adverse effects*
  • Fibrosis
  • Humans
  • Hypertension / etiology*
  • Hypertension / pathology
  • Hypertension / physiopathology
  • Kidney Cortex / blood supply
  • Kidney Cortex / pathology
  • Kidney Diseases / physiopathology
  • Middle Aged
  • Obesity / complications*
  • Sodium Chloride, Dietary / adverse effects*

Substances

  • Sodium Chloride, Dietary