Mild Hypertension: Current controversies and new approaches

These aspects were considered at the symposium "Mild hypertension. Current con troversies and new approaches" held at Titisee in West Germany, October.
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The predominant receptor subtype varies on each cell. For instance, alphareceptors predominate on platelets. This has raised questions about the validity of extrapolating such data to cardiovascular function. To overcome this problem some studies have combined pharmacological and biochemical responses.

Patients with gross sympathetic failure, for example, exhibit exaggerated pressor responses to infused noradrenaline and have increased alpha-receptor binding sites on platelets Davies et al. Depressor responses to baroreceptor stimulation were virtually unaffected, whereas pressor responses to baroreceptor deprivation are only slightly reduced 1.

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In one series of observations 11 , we studied eight subjects before and after intravenous administration of Ilg clonidine. The responses are identical before and after the drug, despite the hypotension produced by it. Skip to content Home. Download e-book for iPad: Current controversies and new approaches by W.

Latest guidelines in the management of hypertension

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The renal-mean arterial pressure set-point model is briefly described to explain that a shift of the pressure natriuresis relationship toward abnormally high pressure levels is a pathophysiological characteristic of essential hypertension. Evidence indicating that this anomaly in the pressure natriuresis relationship arises from a sympathetic nervous system dysfunction is briefly formulated, and the most widely accepted pathophysiologic proposal to explain the development of this sympathetic dysfunction is described, with commentaries about novel action mechanisms of some drugs currently used in essential hypertension treatment.

The overall hypertension prevalence among the adult population was estimated at From this prevalence, it is evident that hypertension is a very important public health challenge because its complications, including cardiovascular, cerebrovascular, and renal diseases, are mayor causes of morbidity and mortality.

Reducing blood pressure in individuals with hypertension prevents or attenuates these complications [ 5 , 6 ].

Mild hypertension in people at low risk

Essential hypertension is currently understood as a multifactorial disease arising from the combined action of many genetic, environmental, and behavioral factors. Given the multifactorial nature of blood pressure homeostasis, any change in blood pressure as, for example, one due to a mutation, is likely to be compensated by feedback, complementary action, or change, in some other control mechanisms, in an effort to return blood pressure to normal.

It is only when the balance between the factor s that tend to increase the blood pressure and those that try to normalize it is sufficiently disturbed, when the compensatory mechanisms fail to counteract the perturbation, that essential hypertension results [ 8 ]. A century of epidemiological, clinical, and physiological research in humans and animals has provided remarkable insights on the relationships existing between dietary salt sodium chloride , renal sodium handling, and blood pressure.

The evidence points to a causal link between a chronically high salt intake and the development of hypertension, when the kidneys are unable to excrete the ingested amount of sodium unless blood pressure is increased [ 9 — 11 ]. In conjunction with this primary causal factor, a number of adjunctive factors, such as obesity, diabetes, aging, emotional stress, sedentary life style, and low potassium intake, may increase the probability of developing hypertension [ 10 , 12 ].

The relative stability of arterial blood pressure leads to the conclusion that it is a highly controlled variable. Arterial pressure is maintained at the level satisfactory to ensure an adequate tissue perfusion.

International Journal of Hypertension

Baroreflexes and vasoactive hormones produce tight regulation over relatively short time spans [ 13 ]. Long-term regulation is, most generally, thought to be achieved through the renal fluid volume regulation mechanism. Regulation of mean arterial pressure MAP requires integrated actions of the physiological systems affecting its major determinants Figure 1 a. Blood flow depends on cardiac output and blood volume, whereas resistance is primarily determined as total peripheral resistance by the contractile state of small arteries and arterioles throughout the body, which is itself determined by the tissues blood flow autoregulation mechanism.

Blood volume depends on extracellular fluid volume ECFV , which itself is determined by the total body sodium content. The latter depends on the balance sodium equilibrium between sodium intake and urinary sodium excretion natriuresis; the main route of body sodium loss.


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Sodium equilibrium is critical to ECFV, and the kidneys, as the principal route through which sodium is eliminated from the body, are therefore central to the long-term stability of MAP. A key component of this feedback is the pressure natriuresis or the effect of arterial pressure on renal sodium and water excretion, exemplified in acute and chronic renal function curves Figure 1 b ; thin and thick curves, resp.

Arterial pressure is set at the level required by the kidney to allow sodium and water excretion to match the intake point A, Figure 1 b. Basal-acute and normal-chronic renal function curves curves 1 and I, resp. Kidney perfusion studies show that, in the absence of a change in sodium intake, a rise in MAP or renal perfusion pressure is matched by increased renal sodium excretion point B; sodium excretion exceeds intake , or pressure natriuresis, which reduces ECFV and cardiac output and returns MAP to normal.

Therefore, disturbances that tend to increase arterial pressure, such as increased peripheral vascular resistance, would cause only a transient increase in arterial pressure, because they would also provoke increased renal sodium excretion.

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Hence, the kidney strives to protect against perturbation from the sodium equilibrium set point, and sodium balance and MAP are maintained by a feedback system displaying infinite gain. That infinite gain is invoked to explain the fact that when sodium intake is increased, renal sodium excretion is similarly increased point C , in response to a very small increase if any in MAP, to attain sodium equilibrium. Again, acute and chronic renal function curves curves 2 and I, resp. When sodium intake is decreased, renal sodium excretion is similarly decreased point D , in response to a very small decrease in MAP.

As expected, acute renal function curve 3 regulatory mechanisms acting to increase renal tubular sodium reabsorption and normal-chronic renal function curve I coincide at the slightly decreased MAP level. If this feedback mechanism is valid, hypertension results from a shift in the renal-pressure natriuresis function to the right chronic renal function curve II , so that a higher pressure is required to attain sodium balance on a normal sodium intake point E. In this condition, the acute renal function curve 3 and the abnormal-chronic renal function curve II coincide at a hypertensive MAP level.


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Hence, the acute renal function curve 3 which corresponds to a situation with regulatory mechanisms acting to increase renal tubular sodium reabsorption is operative, even when sodium intake is normal. In the presence of hypertension, if sodium intake is increased, a higher than normal MAP increase is necessary to obtain sodium balance point F [ 8 , 13 — 15 ]. With the intrinsic kidney function being normal, in the early stage of essential hypertension, an abnormal pressure natriuresis relationship can only result from an abnormal regulation of the kidney function.

If the start of human evolution is arbitrarily set at the beginning of the Paleolithic, during 3 million years, the ancestors of humans, like all other mammals, ate a diet containing little sodium and much potassium: In the Stone Age, the average life span was approximately 30 years. During these times, traits that worked to increase blood pressure with increasing stress would be favorable for survival: Thus, the ability to easily increase blood pressure is a characteristic that might have conferred an evolutionary advantage until modern times [ 10 ].

Blood pressure is directly proportional to total body sodium content. As sodium intake is limited in natural foods, physiological mechanisms to promote sodium ingestion and to prevent sodium loss into urine would have been established early in human evolution [ 23 ]. To promote sodium ingestion, sodium appetite is a motivated behavioral state, arising in response to sodium deficiency that drives humans to seek and ingest food and fluids containing sodium [ 24 ]. In addition, sodium depletion or emotional stress activates the sympathetic nervous system, which, acts mainly via stimulation of the RAAS and further prevents urinary sodium loss [ 25 , 26 ].

Personalized medicine—a modern approach for the diagnosis and management of hypertension

Besides sodium appetite, evolution has provided humans with a pleasant liking of salt taste, which motivates man to ingest sodium in excesse of need, when it is available [ 24 ]. About years ago, humans discovered that salt could be used to preserve food and developed sophisticated techniques for salt production [ 27 , 28 ]. Humans then satisfied their innate taste for salt and have been adding it to food ever since [ 27 , 29 ].

Salt then became of great economic importance as it made it possible to preserve food, allowing the development of cities. Salt was the most taxed and traded commodity in the world [ 30 , 31 ]. However, with the invention of the deep freezer and the refrigerator at the end of the 19th century , salt was no longer required as a preservative. Although preference for salty-tasting food and prevention of sodium loss may once have conferred an evolutionary advantage, ingestion of excessive amounts of sodium now results in chronic hypertension [ 10 , 11 , 24 ].

Many large observational epidemiological investigations conducted worldwide link high salt intake and hypertension [ 30 , 33 ]. Furthermore, populations with low average daily sodium intake some tribal societies which do not add salt to the food had relatively low blood pressure and very little or no increase in blood pressure with age [ 16 ].

However, migration involves more change than just a change in salt intake, because other factors, such as mental stress and changes in physical activity and diet, may contribute to the rise in blood pressure [ 33 ]. Figure 2 a shows that in acculturated populations as the Mexican population , which add salt to the food, systolic and diastolic blood pressure increase with age and that this increase does not occur in nonacculturated populations.

In the same way, in acculturated populations as those of Canada, Mexico, and USA , hypertension prevalence increases with age Figure 2 b [ 3 , 17 , 18 ]. However, blood pressure increase with age is higher in urban than in rural environments, reflecting the environmental influence on blood pressure [ 35 ].

On the other hand, in two clinical studies performed on some individuals in which, within their usual diet, dietary sodium intake was randomly and sequentially adjusted at low 1. In contrast to sodium, potassium was abundant in the fresh food that made up the stone age diet; but, in modern times, diets have shifted drastically to processed foods, reducing potassium intake [ 22 , 31 ]. A low potassium diet induces sodium retention and increases blood pressure [ 38 ]. On the contrary, potassium supplementation promotes natriuresis and decreases blood pressure [ 39 ].

However, because humans have evolved with sodium deficiency for a long time, we have developed a powerful hedonistic taste for salt. This innate desire for salty foods, to which cultural and social habits have superimposed, makes it very hard to drastically reduce sodium intake [ 10 , 42 ]. At the end of the 19th century, the renal sympathetic nerves were known to contain fibers which upon stimulation decreased renal blood flow and urinary flow rate.

It was also known that renal blood flow and urinary flow rate increased after renal sympathetic nerves transection [ 43 ]. In the early decades of the 20th century, faced with the high mortality of severe hypertension and the absence of effective pharmacological therapy, a number of operations on the sympathetic nervous system, such as radical splanchnicectomy, were devised in an attempt to lower blood pressure.

By the late s, most of the available antihypertensives, which by then had been developed, antagonized the sympathetic nervous system. The potency and clinical usefulness of these drugs helped to sustain the argument that the sympathetic nervous system was important in the pathogenesis of essential hypertension [ 44 ]. The sympathetic nervous system exerts a basal excitatory activity over the kidney.