Seasonal Variations in Blood Pressure

Talma Rosenthal, MD

Disclosures

Am J Geriatr Cardiol. 2004;13(5) 

In This Article

Sympathetic Nervous System

The effect of ambient temperature on the sympathetic nervous system has also been studied. Marchant et al.[4] noted that cold increases sympathetic tone, which increases both heart rate and blood pressure and elevates myocardial oxygen demand. A rise in sympathetic activity in cold compared with warm season was noted by Minami et al.[30] and Leppaluoto and Hassi[51] as well.

Several authors demonstrated simultaneous elevation of blood pressure and plasma noradrenaline concentration in response to cold exposure.[52,53,54] Increases in plasma and urinary noradrenaline in winter were observed in patients with essential hypertension.[8,11,55] Hata et al.[8] reported that normal subjects display no seasonal difference in blood pressure, but their levels of urinary sodium and norepinephrine are significantly higher in winter than in summer, whereas patients with essential hypertension show higher values for all three parameters in winter. This rise may be related to increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion.

Feller and Hata's data[56] on increased urinary catecholamines excretion in response to exposure to cold broke down into two groups: an increase mainly in epinephrine excretion in response to acute cold, and an increase mainly in norepinephrine excretion in response to chronic cold exposure. However, cold pressor stimulation in normal subjects generally evokes a rise in arterial blood pressure, heart rate, total vascular resistance, and muscle sympathetic nerve discharge,[57,58] but the increase in plasma noradrenaline levels, an indirect marker of sympathetic nervous response, during the cold pressor test is somewhat inconsistent and appears to depend mainly on the duration of hand immersion in ice water.[58,59]Hiramatsu et al.[60]suggested that the elevation in blood pressure in response to cold was due to norepinephrine.

Urinary collections over 5 years by Yamamoto et al.[61] showed the means and scatters of total metanephrine varied significantly depending on the season of the year: from a mean of 380 mug/d during 3 months of summer to 800 mug/d during 3 winter months. The means of summer and winter months showed minor seasonal variation for vanillylmandelic acid: 3.8 mg/d and 4.5 mg/d, respectively. The results suggest a seasonal difference of catecholamine catabolism.

Keatinge et al.[62] found that cold-evoked sympathetic activation not only elevated blood pressure but also increased platelet count and volume and whole blood viscosity (which increased by 21%). These authors also noted a rise in cholesterol. Kawahara et al.[63] suggested that the increase in sympathetic nervous activity related to cold may serve to enhance platelet function, offering a possible explanation for the risk to essential hypertensives of thrombosis in cold weather.

When Izzo et al.[55] examined seasonal changes they found increased heart rate and total peripheral resistance. They also found decreased cardiac output, suggesting that a cold climate causes sympathetically mediated vasoconstriction leading to an elevation of blood pressure.

Sharma et al.[11] suggested a multifactorial etiology for the rise in blood pressure in winter that combines increased sympathetic nervous activity, evidenced by increased norepinephrine and epinephrine in plasma and urine, and decreased environmental loss of fluids and sodium.

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