Does Being Overweight Cause High Blood Pressure?

There are numerous anomalies linked with obesity-related arterial hypertension, including activation of the neurological system, a heightened sensitivity to renin, and sodium retention.

In this article, we will discuss the Possible Mechanisms by which obesity can lead to elevated arterial pressure, the interaction of obesity with the sequelae of hypertension, and the treatments that are believed to optimally treat obesity-related hypertension.

Pathophysiologic Mechanisms of Obesity

According to the Guyton hypothesis, prolonged hypertension can emerge only when the relationship between arterial pressure and natriuresis is improper (ie, when pressure-natriuresis is disordered or when pressure-natriuresis is deranged). 

If a normal relationship between pressure and renal sodium excretion pertains, increasing pressure will result in greater sodium excretion and a decrease in pressure.

Although the evidence to support this idea is considerable, it must not lead to the assumption that all hypertension arises from disease in the kidney because numerous factors (especially specific hormones) can affect the pressure-natriuresis link in normal kidneys.

The clearest illustration of this is the activity of aldosterone, which includes increased renal tubular salt reabsorption and the formation of hypertension even in patients with normal renal function.

How Overweight and High Blood Pressure is Linked?

In light of this, one may wonder how obesity is linked to high blood pressure.

To put it another way, what effect does obesity have on the link between pressure and natriuresis? Increased blood flow, vasodilation, cardiac output, and hypertension are all connected with obesity.

There is no rise in cardiac index (cardiac output divided by body weight) although the glomerular filtration rate increases. 

Hypertension is also caused by an increase in renal salt retention.

An increase in sympathetic tone, activation of the renin-angiotensin system (RAS), hyperinsulinemia, and structural abnormalities in the kidney are all thought to have a role in the pressure-natriuretic curve modifications caused by obesity. 

Obesity-related hypertension can be prevented by blocking the sympathetic nervous system (combined alpha and beta blocker).

Hypertension can be caused by leptin, a hormone found in fat that reduces calorie intake and increases thermogenesis by stimulating the sympathetic nervous system. 

Sympathetic inhibition is also effective in preventing leptin-induced hypertension.

It is clear from this and previous studies that leptin plays a major role in obesity-induced hypertension by activating the sympathetic nervous system.

In animal models of obesity-related hypertension, renal denervation reduces the development of hypertension, suggesting that the activation of renal nerve traffic and subsequent change of the pressure-natriuretic connection are linked to sympathetic activation.

It’s also possible that hyperleptinemia stimulates the hypothalamic pro-opiomelanocortin pathway in the hypothalamus, resulting in a high sympathetic output. 

The melanocortin pathway directly regulates hypertension and weight, as demonstrated by recent studies of mutations in the melanocortin 4 receptor, which has been shown to cause hypertension in humans.

Despite increased sodium retention in the kidney, the RAS is activated in hypertension by elevated levels of circulating renin, angiotensinogen, and angiotensin II.

RAS activation is not fully known, however, angiotensinogen syntheses in fat tissue provide a possible indication as to the cause. 

When angiotensinogen levels rise above the renin reaction’s rate constant, it causes an increase in angiotensin I production, which then leads to an increase in angiotensin II.

Obesity-related increases in renin activity could be the result of heightened sympathetic nervous system activation.

The sodium-retention hormone aldosterone is synthesized when levels of angiotensin II, which is produced by the kidneys, are elevated. 

Obesity is also linked to an increased risk of hyperinsulinemia. Insulin may assist maintain raised blood pressure by increasing salt reabsorption in the tubules under certain conditions.

Angiotensin-converting enzyme inhibitors and peroxisome proliferator-activated receptor-gamma agonists indirectly support the participation of the RAS and hyperinsulinemia in this process. 

The endocannabinoid system may play a role in obesity and hypertension. Endocannabinoid levels in tissues and the bloodstream are elevated in obese individuals.

It is notable that the inverse cannabinoid receptor 1 agonist rimonabant and taranabant produce weight reduction as well as alleviate obesity-related metabolic problems, suggesting a function for endocannabinoids in obesity and perhaps hypertension. 

Obesity-induced structural alterations in the kidney are also thought to be important.

An additional cause of renal sodium reabsorption problem has been identified as a result of the increased abdominal pressure caused by obesity. Renal tubule glycoprotein deposition may also play a role.

In addition, obesity-related hyperfiltration sets the foundation for glomerular and renal function decline, as well as accompanying elevations in blood pressure.

Why Does Weight Affect Blood Pressure?

Hypertension is related to well-known sequelae, including coronary cerebrovascular illness, artery disease, renal insufficiency, atherosclerosis, atrial fibrillation, left ventricular hypertrophy, and congestive heart failure. 

Because obesity-related hypertension predisposes to these diseases, it is no different.

However, there seem to be subtle distinctions between the sequelae observed in obese vs lean persons with hypertension.

Indeed, the so-called obesity paradox has recently been identified, suggesting that, while obese patients are more prone to have cardiovascular structural abnormalities, they may have greater survival than lean individuals with hypertension.

Although disputed, this hypothesis is intriguing, as is the notion that obese patients with hypertension may have an increased risk of renal insufficiency. 

The Framingham Heart Study found that hypertension is linked to an increased chance of left ventricular hypertrophy, which is a potent risk factor for cardiovascular death. 

As a result of obesity’s increased intravascular capacity, cardiac output increases. Concentric adaptive hypertrophy is a side effect of high blood pressure.

As a result, obese people with high blood pressure have both concentric and eccentric left ventricular hypertrophy.

Eccentric hypertrophy, a form of left ventricular hypertrophy in which the ventricular diameter remains the same but the left ventricular wall thickness increases, is common in obese individuals (to be contrasted with concentric hypertrophy typically seen in the lean individual with hypertension that is associated with the decreased ventricular diameter and increased wall thickness). 

It has recently been researched extensively in the Bogalusa Heart Study, and it was revealed that obesity and eccentric hypertrophy are linked in young people.

Even more intriguing are the findings of a recent large-scale investigation on the heart geometry of lean and obese patients with hypertension.

Cardiology research at Ochsner Medical Center has shown the following: 

Patients who were obese were more likely to have abnormal LV [left ventricular] geometry than those who were not fat (49 percent vs. 44 percent, p 0.0001 for the four patterns). 

In obese patients, CR [concentric remodeling] was the most common aberrant pattern, with eccentric and concentric LV hypertrophy occurring in just 7% and 8%, respectively (32 percent, 6 percent, and 6 percent, respectively).

More than half of obese people died before the age of 65, compared to one in six non-obese people.

Excentric and concentric LV hypertrophy caused gradual increases in mortality in both groups when compared to individuals with normal cardiac structures (obese patients 2.8 percent, 4.8 percent, 5.3 percent, and 6.9 percent, respectively; and non-obese patients 4.3 percent, 8.4 percent, 9.6 percent, and 11.8 percent, respectively). 

In other words, here’s the paradox of obesity (i.e., lower mortality in obese as opposed to lean individuals with hypertension).

Accordingly, if the obesity paradox is real, the question arises as to whether obesity-related hypertension can account for the variations in mortality or whether other minor abnormalities in cardiovascular sequelae are at play. 

The transcriptome (the pattern of gene expression) of patients with left ventricular hypertrophy is being studied as an indirect means of answering this question. 

There are different gene expression patterns in the left ventricle of dogs fed a high-fat diet that induces obesity, including an increase in the transforming growth factor-beta pathway.

Because angiotensin II has already been shown to increase transforming growth factor-beta and the RAS, this is a significant finding.

It’s possible that similar investigations could provide insight into the genetic basis of the obesity conundrum. 

Obesity and hypertension have been linked to an increased risk of renal failure, according to extensive research.

Because of the pathophysiologic mechanisms mentioned above, obesity-related hypertension can be caused by hyperfiltration, RAS activation, and kidney structural changes that are all caused by weight gain.

The impacts of obesity-related glucose intolerance and diabetes mellitus must also be considered.

Thus, obesity plus diabetes and hypertension are a formidable and deadly combo when it comes to renal function.

Indeed, these three causes may be at the root of the recent surge in the prevalence of chronic renal illness.

How to Lose Weight with High Blood Pressure?

Obesity-related hypertension is treated largely in the same way as other forms of high blood pressure, but with a focus on food.

Lifestyle and nutritional changes, as well as medication, are still the conventional treatment for a wide range of conditions.

Here, we will not go into great detail about the many therapy options available to you. The treatment of patients with obesity-related hypertension, however, can benefit from some principles. 

First and first, weight loss must be the focus of therapy. Obesity-related hypertension must be treated with a primary focus on weight loss, however, how challenging this may be.

As a result of losing weight, many of the pathophysiologic mechanisms that contribute to high blood pressure will be reversed.

At the very least, it is possible to reverse some structural derangements and reduce the likelihood of them progressing further. 

It’s possible that diuretic therapy in an obese patient could exacerbate glucose intolerance or perhaps lead to frank diabetes, increasing the risk even more.

Glucose and blood pressure control are both effective in persons with diabetes. Both have to be accomplished.

That’s why hypertension therapy should be aimed at improving glucose metabolism rather than deteriorating it.

A deterioration in glucose tolerance has been linked to the beta sympathetic blockade, whereas postural hypotension and other side effects have been linked to alpha sympathetic blockade. 

Glucose tolerance is not worsened and may even be improved when the RAS is interrupted, and this is usually well tolerated. RAS disruption is not without risk, though.

Angiotensin-converting enzyme inhibition can cause angioedema, and all medicines that interfere with the RAS must be stopped during pregnancy.

While this family of medications is efficacious and well-tolerated in this patient population, they typically need to be combined with agents from other pharmacological classes to achieve control of arterial pressure. 

In the future, newer agents may play a role. Proliferator-activated receptor-gamma antagonists enhance insulin resistance and in certain circumstances lower arterial pressure.

Telmisartan, an angiotensin receptor blocker, has been demonstrated to have some intrinsic peroxisome proliferator-activated receptor-gamma activity, and it could prove valuable to many patients if further studies verify its efficacy.

Also, endocannabinoid blockers could be useful. Although the cannabinoid receptor 1 receptor blocker rimonabant decreased blood pressure in overweight humans, it increased the heart rate of rats.

There is some evidence to support the use of cannabinoid inhibitors in the treatment of renal vascular injury, based on these findings. 

Until we know more about these fresh agents, we can’t say for sure what their role will be.

Final Words

It has only recently been realized that obesity increases the risk of hypertension and changes the progression of hypertensive cardiovascular disease.

Obesity and diabetes have a long history of co-occurring, which makes diagnosing and treating individuals with either of these diseases more difficult. 

Regardless of how tough it may be, the first step in any treatment plan should always be to reduce one’s weight.

Pharmacotherapy helps lower blood pressure, but it must be taken with caution to prevent deterioration of glucose tolerance. 

However, the true utility of these newer agents has yet to be demonstrated. Newer medicines promise greater management of arterial pressure, weight, and metabolic parameters.

Obesity-related hypertension can be better treated with pharmacological therapy if researchers continue to investigate the pathways that lead to this condition.